Indeed, IGF1 stimulated an increase in protein levels of rapamycin-insensitive companion of mammalian target of rapamycin (Rictor), one of the main components of mTORC236, and an increase of pAKTS473 in BCR-ABL1+ BA/F3 (Fig. 5A) and primary murine B-ALL cells (Fig. 5B), but not in empty vector+, MLL-AF9+ (BA/F3) or primary murine MLL-AF9+ AML counterparts. This evidence concerns the gene BCR and acute myeloid leukemia.