To expand our studies to other oncogene-driven AKT-activated leukemia cell models, we chose leukemia cell lines with known gain-of-function tyrosine kinase mutations, which are prevalent in 30-40% of patients with AML (FLT3 and KIT) or ALL (BCR-ABL1 and FLT3) [2]: The acute monocytic leukemia cell line MOLM14 (harboring a FLT3 ITD mutation) and the CML blast crisis cell line K562 (harboring a BCR-ABL1 fusion transcript mutation) were exposed to NVP-BGT226 in a dose dependent manner and inhibition of cellular proliferation was determined. This evidence concerns the gene AKT1 and acute lymphoblastic leukemia.