In a recent study, Estruch et al.[68] applied a genetically modified inv(16)/KITD816Y AML mouse model, mimicking AML patients with constitutive mutational KIT-dependent activation of the PI3K/AKT signaling pathway, to explore the therapeutic efficacy of standard AML chemotherapy in combination with DDR or PI3K/AKT inhibitors (i.e., DNA-PKi/NU7026 or pan-PI3Ki/BKM120). The gene discussed is KIT; the disease is acute myeloid leukemia.