Using GAB2 deficient mice [6], we previously showed that GAB2 serves as an important effector of the oncogenic FLT3-ITD receptor tyrosine kinase in acute myeloid leukemia (AML) [7, 8] and of BCR::ABL1 in CML [9–12]. This evidence concerns the gene BCR and chronic myelogenous leukemia, BCR-ABL1 positive.