Gsk3a/b knockdown (20) or Gsk3b deletion (21) in mouse bone marrow causes a pronounced myeloproliferative phenotype, and Gsk3a/b double-knockout (DKO) causes marked expansion of both mature granulocytes and primitive blasts, leading to an aggressive AML (21), but the substrates that mediate GSK-3 functions in mouse and human hematopoietic malignancies have not been extensively characterized. The gene discussed is GSK3A; the disease is acute myeloid leukemia.