In the bone-marrow microenvironment, while IGF-1 provided by stromal elements is a well-established driver of myeloma growth and survival via IGF1R-PI3K/ERK signaling (34, 35)and direct IGF1R dephosphorylation by PTPRG has not been demonstrated, PTPRG dephosphorylates and dampens collaborating RTKs (e.g., FGFR family members), thereby possibly lowering shared adaptors (FRS2-RAS–MAPK; PI3K–AKT) (40) and tuning the effective gain of IGF1R signaling. Here, AKT1 is linked to plasma cell myeloma.