HOXA9 and acute myeloid leukemia: However, retroviral overexpression in HSCs of the homeobox proteins HoxA9 and Meis1a (downstream players in numerous pathways found deregulated AML) or double Idh2R140Q/Flt3-ITD transgenic animals did recapitulate AML features, strengthening the conclusion that Idh2 mutations require additional genetic events to cause leukemic transformation.