Gab2 Deficiency Prevents Flt3-ITD Driven Acute Myeloid Leukemia In Vivo

Utilizing a Flt3-ITD knock-in, Dnmt3a haploinsufficient mouse model, researchers demonstrated that Gab2 was essential for the development of Flt3-ITD driven acute myeloid leukemia in vivo, asGab2 deficient mice displayed prolonged survival, presented with attenuated liver and spleen pathology and reduced blast counts.