MV4-11 acute myeloid leukemia cells express constitutive STAT5 activity as a consequence of an internal tandem duplication (ITD) mutation in the FLT3 receptor tyrosine kinase, another Hsp90 client protein [42] and, as such, represent an alternative model of STAT-driven oncogenesis. This evidence concerns the gene SOAT1 and acute myeloid leukemia.