If convergent assembly of MYB with common transcription factors in biologically diverse subtypes of AML is responsible for the induction of oncogenic gene expression and blockade of normal hematopoietic differentiation, then pharmacologic blockade of this process would suppress shared gene expression programs associated with AML growth and survival, and promote gene expression programs associated with hematopoietic differentiation. The gene discussed is MYB; the disease is acute myeloid leukemia.