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, BAP1 is linked to nonpapillary renal cell carcinoma.