We then hypothesized that there is differential oncogene- and/or lineage-dependent sensitivity of leukemias to mTORC2 signaling downstream of the IGF1R, which may explain the observed phenotypes of CML, B-ALL and AML in ANXA2 KO mice. This evidence concerns the gene ANXA2 and chronic myelogenous leukemia, BCR-ABL1 positive.