To ascertain whether the observed changes in autophagic flux were indeed correlated with SRC activity, we performed experiments modulating SRC activity by either inhibiting (by siRNA knockdown or by treatment with dasatinib, a SRC inhibitor) or overexpressing SRC (using a V5-tagged SRC construct) in BAP1-deficient ccRCC UMRC-6 cells. Here, SRC is linked to nonpapillary renal cell carcinoma.