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  7. Hematopoiesis Diagrams for EHA 2026 Researchers
Tutorials·2026-05-22·17 min read

Hematopoiesis Diagrams for EHA 2026 Researchers

Draw publication-ready hematopoiesis diagrams for EHA 2026 posters: classical tree, bone marrow niche, JAK/STAT pathway, AML block, and AI prompts.

SciFig Team

SciFig Team

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On this page

  • 1. Why Hematopoiesis Diagrams Anchor Almost Every EHA Poster
  • 2. The Classical Hematopoiesis Tree: From HSC to 11 Mature Lineages
  • 3. Myeloid vs Lymphoid: The First Major Branching Point
  • 4. Key Intermediate Progenitors: CMP, GMP, MEP, CLP
  • 5. The Bone Marrow Microenvironment: Niche Anatomy for Stem Cell Posters
  • 6. Signaling Pathways Controlling Hematopoiesis: JAK/STAT, Wnt, Notch, SCF-c-Kit
  • 7. Disrupted Hematopoiesis in Disease: AML, MDS, MPN, Bone Marrow Failure
  • 8. AI-Powered Hematopoiesis Diagrams: SciFig Workflow for Stem Cell Posters
  • 9. Free Trial CTA + Related Reading: 5 Copy-Paste Hematopoiesis Prompts
  • FAQ

You start with the hematopoietic stem cell at the top, branch down through multipotent progenitor, then myeloid and lymphoid commitment, and somewhere around the granulocyte-monocyte progenitor your figure stops making biological sense. GPT image insists on drawing the megakaryocyte branching off from CLP. Midjourney inverts the myeloid-lymphoid split. A bright label appears reading "CD34+ E-progenitor" — a cell type that does not exist. You re-roll, and the next version puts erythrocytes under the lymphoid lineage. After 40 minutes you give up and trace a textbook tree by hand in Illustrator.

This is the moment that derails most stem cell and hematologic malignancy posters at EHA. The hematopoiesis tree is the most foundational figure in hematology — the orientation map every reviewer expects before they engage with your science — and the single figure where generic AI image models fail most consistently because the topology is unforgiving. One inverted branch and the entire lineage reasoning collapses. This guide walks through the classical hematopoiesis tree from HSC to 11 mature lineages, the bone marrow niche architecture, the signaling pathways that govern self-renewal versus differentiation, the disease states where hematopoiesis breaks down, and the AI-assisted workflow that gets the topology right on draft one.

Hematopoiesis tree: HSC → MPP → CMP (myeloid) and CLP (lymphoid) lineages → 11 mature blood cell types (Figure generated with SciFig)
Hematopoiesis tree: HSC → MPP → CMP (myeloid) and CLP (lymphoid) lineages → 11 mature blood cell types (Figure generated with SciFig)

Transparency note: Illustrations in this article were generated with SciFig AI and reviewed by the author for scientific accuracy. Cited claims link to peer-reviewed sources, NIH educational materials, and the ASH Education Book.

1. Why Hematopoiesis Diagrams Anchor Almost Every EHA Poster

Walk through any EHA poster session and you will see a simplified hematopoiesis tree in the introduction panel of nearly every stem cell, leukemia, lymphoma, myeloma, or transplantation poster. The reason is conceptual: hematology operates on a shared mental model of where each cell type comes from, and your study is implicitly a claim about which point in that lineage you are intervening on. If you cannot show the tree clearly, you cannot show your study clearly.

The EHA 2026 program lists Hematopoiesis, stem cells and microenvironment as a Tier 2 abstract topic — broad enough to span the annual Molecular Hematopoiesis Workshop, which on June 11 will cover stem cell biology, hematologic malignancies, signaling, developmental hematopoiesis, inflammation, the epigenome, aging, clonal hematopoiesis, gene therapy, metabolism, the microenvironment, and novel technologies. Every one of those subtopics needs hematopoiesis context figures. This guide covers the six most universal ones.

2. The Classical Hematopoiesis Tree: From HSC to 11 Mature Lineages

The classical hematopoiesis tree starts with the hematopoietic stem cell (HSC) — a long-term self-renewing cell that sits quietly in the bone marrow niche. The HSC gives rise to a multipotent progenitor (MPP), which loses self-renewal capacity but retains broad lineage potential. From MPP, the tree bifurcates: the common myeloid progenitor (CMP) gives rise to all myeloid lineages; the common lymphoid progenitor (CLP) gives rise to all lymphoid lineages. The 11 mature lineages, by convention, are: erythrocytes, megakaryocytes (platelets), neutrophils, eosinophils, basophils, monocytes/macrophages, dendritic cells, mast cells, NK cells, B cells, and T cells.

This is the topology, but the actual figure is unforgiving. The myeloid branch must give rise to erythrocytes and megakaryocytes through the megakaryocyte-erythroid progenitor (MEP); the lymphoid branch must not. Mast cells and dendritic cells have complicated dual origins that most figures simplify. Authoritative reference points: the NIH dictionary entry on hematopoiesis and the ASH publications portal on hematopoiesis education provide consistent topology that you can match your figure against.

The visual literacy bar is high because every reviewer in the hall has seen this tree a thousand times. Yours has to either match the canonical topology with publication-grade clarity, or — if your study addresses a specific lineage decision point — be annotated to highlight exactly where in the tree your intervention lives.

3. Myeloid vs Lymphoid: The First Major Branching Point

The CMP-CLP split from MPP is the most consequential branching decision in hematopoiesis, and it is also where generic AI image models most often invert the topology. Get this wrong and every downstream lineage is mislabeled.

The split is regulated by competing transcription factors — PU.1 favors myeloid commitment, while Ikaros and E2A favor lymphoid commitment. The two daughter populations have fundamentally different downstream fates: CMP gives rise to red cells, platelets, granulocytes, monocytes, mast cells, and most dendritic cells; CLP gives rise to T cells, B cells, NK cells, and plasmacytoid dendritic cells. A figure that mixes these is not a stylistic choice; it is a topology error that an experienced reviewer will spot before reading your title.

For posters addressing acute myeloid leukemia, the myeloid branch needs to be expanded with intermediate progenitors (CMP → GMP → myeloblast → granulocyte/monocyte). For posters addressing T-cell or B-cell malignancies, the lymphoid branch needs the thymic and bone marrow lymphoid trajectories drawn separately.

4. Key Intermediate Progenitors: CMP, GMP, MEP, CLP

Below MPP, the four most important intermediate progenitors are CMP, GMP, MEP, and CLP. These are the "named gates" in hematopoiesis — each is defined by a specific combination of surface markers (most commonly CD34, CD38, CD45RA, CD123, CD135/Flt3) and downstream lineage potential.

  • CMP (common myeloid progenitor) — CD34+CD38+CD123+CD45RA−. Gives rise to GMP and MEP.
  • GMP (granulocyte-monocyte progenitor) — CD34+CD38+CD123+CD45RA+. Gives rise to neutrophils, eosinophils, basophils, monocytes, mast cells, and conventional dendritic cells.
  • MEP (megakaryocyte-erythroid progenitor) — CD34+CD38+CD123lowCD45RA−. Gives rise to erythrocytes and megakaryocytes/platelets.
  • CLP (common lymphoid progenitor) — CD34+CD38+CD7+CD10+CD45RA+. Gives rise to T cells, B cells, NK cells, and plasmacytoid dendritic cells.

A precise figure annotates each intermediate with its surface marker phenotype and downstream lineages. Sloppy figures — and many AI-generated drafts — invent intermediate names that do not exist (e.g., "CD34+ E-progenitor" or "early myeloid blast") that signal to reviewers you do not know the canonical taxonomy.

5. The Bone Marrow Microenvironment: Niche Anatomy for Stem Cell Posters

The bone marrow niche is the physical and molecular environment where HSCs live, divide, and decide whether to self-renew or differentiate. The canonical reference is the Morrison and Scadden 2014 Nature review on the bone marrow niche for haematopoietic stem cells, which formalized the modern model of overlapping vascular, perivascular, and osteoblastic compartments.

The three niche compartments your figure should distinguish:

  • Vascular niche — Near sinusoidal endothelium. Provides oxygen and signaling cues for active HSCs in cycle.
  • Perivascular niche — Mesenchymal stromal cells (MSCs) and CXCL12-abundant reticular (CAR) cells around vessels. The major source of CXCL12 (SDF-1) that anchors HSCs.
  • Osteoblastic niche — Near the bone surface. Historically associated with HSC quiescence, although the modern model emphasizes vascular/perivascular more than the older "endosteal" view.
Bone marrow niche: sinusoidal vascular, perivascular MSCs and CAR cells, osteoblastic surface, sympathetic nerves (Figure generated with SciFig)
Bone marrow niche: sinusoidal vascular, perivascular MSCs and CAR cells, osteoblastic surface, sympathetic nerves (Figure generated with SciFig)

Sympathetic nerve fibers add a fourth regulatory layer by controlling circadian HSC egress into the bloodstream. For posters addressing mobilization (G-CSF, plerixafor) or trafficking, this is essential to show. For posters addressing AML or MDS, the niche figure should also include the leukemic stem cell perspective — how malignant HSCs co-opt the niche and outcompete normal HSCs.

6. Signaling Pathways Controlling Hematopoiesis: JAK/STAT, Wnt, Notch, SCF-c-Kit

Four signaling pathways dominate hematopoietic regulation, and each shows up frequently in EHA posters either as a normal regulator or as a disease driver.

  • SCF-c-Kit — Stem cell factor binding the c-Kit receptor (CD117) drives HSC survival and early lineage decisions. KIT mutations are central to systemic mastocytosis.
  • Thrombopoietin (TPO)-MPL → JAK/STAT — TPO binding MPL activates JAK2, which phosphorylates STAT3/STAT5; the phosphorylated STAT dimers translocate to the nucleus and activate transcription of self-renewal and survival genes. JAK2 V617F mutation drives myeloproliferative neoplasms.
  • Wnt/β-catenin — Canonical Wnt signaling supports HSC self-renewal; aberrant activation contributes to leukemic transformation.
  • Notch — Notch-Delta interactions drive T-cell lineage commitment in the thymus; aberrant Notch signaling drives T-ALL.
HSC signaling: SCF-c-Kit, TPO/JAK-STAT, Wnt/β-catenin, Notch — controlling self-renewal vs differentiation (Figure generated with SciFig)
HSC signaling: SCF-c-Kit, TPO/JAK-STAT, Wnt/β-catenin, Notch — controlling self-renewal vs differentiation (Figure generated with SciFig)

The JAK/STAT cascade is where AI image models most often invert the direction of signal flow. The canonical sequence is: cytokine binds receptor → receptor-associated JAK kinases trans-phosphorylate → JAKs phosphorylate STAT tyrosine residues → phosphorylated STATs dimerize via SH2 domain interactions → dimer translocates to nucleus → transcription. Generic AI generators frequently draw STAT entering the nucleus first and then dimerizing, which is the wrong order — a clear sign to a reviewer that the figure was generated without molecular biology supervision.

7. Disrupted Hematopoiesis in Disease: AML, MDS, MPN, Bone Marrow Failure

Most EHA disease-focused posters need a figure showing where hematopoiesis breaks down in their specific disease. Four high-frequency examples cover most of the program.

AML (Acute Myeloid Leukemia) — Differentiation block at the myeloblast stage with blast accumulation in the bone marrow. Driver mutations include FLT3-ITD, NPM1, IDH1/2, and TP53. The 2022 ELN/Döhner et al. Blood diagnosis and management framework defines the molecular classification used in current clinical practice.
MDS (Myelodysplastic Syndromes) — Ineffective hematopoiesis with dysplastic morphology, peripheral cytopenias, and increased risk of transformation to AML. Often arises from clonal hematopoiesis of indeterminate potential (CHIP) accumulating over decades.
MPN (Myeloproliferative Neoplasms) — Driver mutations in JAK2 V617F (the most common, ~95% of polycythemia vera; 50-60% of essential thrombocythemia and primary myelofibrosis), CALR, or MPL produce constitutive JAK/STAT signaling and overproduction of erythroid, megakaryocytic, or granulocytic lineages. The Levine et al. 2007 Nat Rev Cancer review on JAK2 in MPN remains a definitive reference.
Bone marrow failure and aplastic anemia — HSC depletion from autoimmune attack, inherited mutations, or environmental insult. The niche is intact but empty.
DiseaseHematopoiesis DefectPrimary Driver MutationsWhere in the Lineage
AMLDifferentiation block at myeloblastFLT3-ITD, NPM1, IDH1/2, TP53Myeloid commitment downstream of CMP/GMP
MDSIneffective hematopoiesis + cytopeniasDNMT3A, TET2, SF3B1, ASXL1HSC/MPP with multi-lineage involvement
MPNOverproduction of mature myeloid lineagesJAK2 V617F (~95% PV), CALR, MPLHSC with JAK/STAT hyperactivation
CHIP/CCUSClonal expansion without overt diseaseDNMT3A, TET2, ASXL1HSC; precursor state to MDS/AML
Aplastic anemiaHSC depletion → empty marrowOften acquired/autoimmune (PNH overlap)HSC pool collapse

Tip

For posters comparing two or more of these disease states (e.g., MDS-to-AML progression or CHIP-to-MDS evolution), build a single shared lineage figure with the lesion point of each disease annotated as a colored highlight rather than drawing each disease's lineage separately. Reviewers absorb the shared scaffold faster, and you reuse the same SciFig source figure across multiple poster panels.
AML differentiation block: myeloid maturation arrested at myeloblast with FLT3-ITD, NPM1, IDH1/2, TP53 mutations (Figure generated with SciFig)
AML differentiation block: myeloid maturation arrested at myeloblast with FLT3-ITD, NPM1, IDH1/2, TP53 mutations (Figure generated with SciFig)
MPN pathogenesis: JAK2 V617F in HSC → constitutive JAK/STAT signaling → PV, ET, PMF lineage overproduction (Figure generated with SciFig)
MPN pathogenesis: JAK2 V617F in HSC → constitutive JAK/STAT signaling → PV, ET, PMF lineage overproduction (Figure generated with SciFig)
For posters addressing clonal hematopoiesis specifically, the disease spectrum extends from CHIP (mutated HSC clones detectable in healthy aging) to CCUS (clonal cytopenias of undetermined significance) to MDS to AML — a continuum that should be visualized as a progression timeline. The Jaiswal and Ebert 2019 Science review on CHIP frames this clinically.
Clonal hematopoiesis progression: CHIP → CCUS → MDS → AML with DNMT3A, TET2, ASXL1 driver mutations over age (Figure generated with SciFig)
Clonal hematopoiesis progression: CHIP → CCUS → MDS → AML with DNMT3A, TET2, ASXL1 driver mutations over age (Figure generated with SciFig)

8. AI-Powered Hematopoiesis Diagrams: SciFig Workflow for Stem Cell Posters

Here is the part where the hematopoiesis tree, the niche figure, and the disease lineage diagrams go from "blocking your week" to "drafted before lunch" — and it is also where you find out why generic AI is structurally inadequate for this specific kind of figure.

If you have already tried generating a hematopoiesis tree with GPT image or Midjourney, you have probably seen the result: the model gets the rough vertical layout but inverts the myeloid-lymphoid split, or it puts the megakaryocyte under CLP, or it generates a confidently-labeled "CD34+ E-progenitor" cell type that does not actually exist in any taxonomy. You re-roll, and the next version has the topology mostly correct but loses the niche cell labels, or it draws erythrocytes branching off the lymphoid lineage. This is not a problem with one specific vendor — no generic image model today can reliably get the hematopoiesis topology right on the first try, because the model is interpreting "tree of blood cells" visually without understanding that one inverted branch invalidates the entire lineage reasoning. And for a hematology poster, a tree with one wrong branch is worse than no tree — it actively misleads the reviewer about the cell biology you are studying.
SciFig is built for exactly this gap. Best-in-class image generation models bring the first-pass tree to a high-fidelity starting point — the HSC → MPP → CMP/CLP topology, the major intermediate progenitors, the 11 mature lineages — most of which is correct on draft one. But for the precision details that matter most — verifying CMP descends from MPP and not from CLP, confirming MEP gives rise to erythrocytes and megakaryocytes, checking that the JAK/STAT cascade flows in the right direction (cytokine → JAK → STAT phosphorylation → dimerization → nuclear translocation) — an editable vector canvas in the browser lets you click any progenitor label and rename it, drag any branch and reposition it, fix one arrow without rerolling the entire tree. The remaining precision gap closes in seconds, not minutes. And the entire workflow stays inside SciFig — one-click export to editable PPTX for your lab meeting, layered SVG for downstream editing, or 8K PNG for A0 poster printing without artifacting. There is no roundtrip to Illustrator to "fix the tree topology" because you fix it in place where it was generated.

Here is the path. Copy this prompt verbatim into SciFig's Text-to-Figure tool to start the classical hematopoiesis tree:

Comprehensive hematopoiesis differentiation tree starting from
hematopoietic stem cell (HSC) at top, branching to multipotent
progenitor (MPP), then bifurcating into common myeloid progenitor
(CMP) on the left and common lymphoid progenitor (CLP) on the right.
CMP gives rise to MEP (erythrocytes, megakaryocytes/platelets) and
GMP (neutrophils, eosinophils, basophils, monocytes/macrophages,
dendritic cells, mast cells). CLP gives rise to T cells, B cells,
NK cells. Vertical layout, color-coded by lineage, accurate cell
morphology, publication-ready style.
Adjust to your study — collapse lineages you are not addressing, expand intermediate progenitors that are central to your work, annotate the specific lineage decision point your intervention targets. The model produces a starter tree in seconds; the SciFig vector canvas lets you refine each progenitor label individually without rerolling.

For the bone marrow niche, the JAK/STAT pathway, the AML differentiation block, the MPN JAK2 figure, and the CHIP evolution timeline — copy the prompts in Section 9 below.

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9. Free Trial CTA + Related Reading: 5 Copy-Paste Hematopoiesis Prompts

The five remaining SciFig prompts for the figures shown in this article. Copy any of them directly into Text-to-Figure:

Hematopoiesis tree — see Section 8 above.
Bone marrow niche:
Cross-section of bone marrow microenvironment showing HSC niche:
vascular niche near sinusoids with endothelial cells, perivascular
niche with mesenchymal stromal cells (MSC) and CXCL12-abundant
reticular (CAR) cells, osteoblastic niche near bone surface,
sympathetic nerve fibers regulating egress. HSC quiescence vs
mobilization shown.
HSC signaling pathways:
HSC self-renewal vs differentiation signaling: SCF-c-Kit, Wnt/β-catenin,
Notch, JAK/STAT (TPO-MPL), TGF-β quiescence. Show cell membrane,
cytoplasmic cascade, nuclear transcription factors (GATA1, PU.1,
RUNX1 lineage commitment). Annotate signaling direction with arrows.
AML differentiation block:
AML pathogenesis: normal myeloid differentiation arrow blocked at
myeloblast stage. Show accumulation of CD34+ blasts in bone marrow,
compared to healthy hematopoiesis. Key mutations annotated:
FLT3-ITD, NPM1, IDH1/2, TP53.
MPN JAK2 V617F:
Myeloproliferative neoplasm pathogenesis: JAK2 V617F gain-of-function
mutation in HSC produces constitutive JAK/STAT signaling, leading to
overproduction of erythroid, megakaryocytic, and granulocytic
lineages. Show resulting PV (polycythemia vera), ET (essential
thrombocythemia), and PMF (primary myelofibrosis) phenotypes.
Clonal hematopoiesis evolution:
Clonal hematopoiesis progression: CHIP (clonal hematopoiesis of
indeterminate potential) → CCUS (clonal cytopenias of undetermined
significance) → MDS → AML. Show clonal expansion of mutated HSC
over age, with DNMT3A, TET2, ASXL1 driver mutations annotated.
Horizontal timeline format.
A new SciFig account starts with 150 starter credits plus 50 refill credits every day. The six figures in this article — hematopoiesis tree, niche, signaling, AML block, MPN, CHIP evolution — typically consume 50–80 credits with iteration. Your starter pack covers the full hematopoiesis figure set plus daily refill margin for refinement. See the pricing page if you anticipate building figures for multiple posters across the year.
For the basics of EHA poster format and the four presentation tiers, start with EHA 2026 poster guidelines and template. For the design principles that distinguish a winning poster from an average one, see how to design a winning EHA 2026 poster. If your work also touches CAR-T cellular immunotherapy targeting hematologic malignancies, the companion piece how to illustrate CAR-T mechanism for EHA 2026 posters covers the engineered T-cell side of the same disease space.
For the layered approach to building any cell signaling pathway figure (including the JAK/STAT and Notch cascades referenced above), see our walkthrough on creating cell signaling pathway diagrams with AI.

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Disclaimer: This article is educational content focused on scientific figure design for conference posters and publications. It is not medical advice and should not be used for clinical decisions. The disease mechanisms, drug indications, and treatment protocols described here are summarized from peer-reviewed sources cited above; for clinical practice, consult primary literature, official treatment guidelines (e.g., NCCN / ESMO / ASH), and licensed clinicians. SciFig is a scientific illustration tool — it does not diagnose, treat, or advise on patient care.
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