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. This evidence concerns the gene FLT3 and acute myeloid leukemia.