Our mechanistic model (Figure 1) elucidates how venetoclax-HMA synergy transcends direct leukemic cell killing: venetoclax counteracts BCL-2-mediated survival signals in FLT3-ITD + clones (↓p-STAT5 by 62%, p = 0.007), while azacitidine upregulates endogenous retroviral antigens, potentiating the graft-versus-leukemia (GVL) effects without GVHD exacerbation. Here, FLT3 is linked to leukemia.