Taken together with previous work, this study highlights the interplay between PP2A and oncogenic kinases including BCR-ABL [22], c-KIT [23] and FLT3, indicating that functional inactivation of PP2A may represent a crucial event in the initiation and conservation of leukemia growth and survival, and likely other cancers driven by oncogenic activation of tyrosine kinases. The gene discussed is FLT3; the disease is leukemia.