AML cells with FLT3-ITD are characterized by predominant expression of an underglycosylated, or high-mannose, 130 kDa FLT3 species that is retained in the ER and mediates aberrant signaling of STAT5, and the serine/threonine kinase Pim-1 is trancriptionally upregulated downstream of STAT5. The gene discussed is PIM1; the disease is acute myeloid leukemia.