Examination of the MERTK control of this SAV1 mechanism revealed that when endogenous SAV1 was depleted, MERTK inhibition, which suppressed Akt activation (Fig. 2e, f) now failed to efficiently suppress Akt activation (Fig. 4e and Supplementary Fig. 13c), and these cells were more resistant to MERTK inhibition-mediated growth suppression (Fig. 4f, g), suggesting that SAV1 may be a major downstream effector of MERTK survival signaling in neoplasia and may be a marker to assess whether MERTK inhibition will be effective. The gene discussed is MERTK; the disease is neoplasm.