Thus, the efficacy of AX in Bcr-AblT315I mutant CML might be explained by its on-target action as a selective inhibitor for this gatekeeper mutant [19] and by “off-target” effects eliminating back-up pathways leading to Gab2 tyrosine phosphorylation and downstream signaling. This evidence concerns the gene GAB2 and chronic myelogenous leukemia, BCR-ABL1 positive.