Immunoblot analysis demonstrated that the aberrant accumulation of free ATG12 protein and of the additional ATG12-containing complex can be observed in all RCC cells deficient for SETD2, i.e., A498, Caki-1, and RCC-FG2 RCC cells, and that the VHL status of the cells did not impact in the acquisition of these characteristics suggesting that the phenotype observed is clearly due to SETD2 deficiency and VHL does not play role on ATG12 regulation (Fig. 4a and Supplementary Fig. 3c, d). Here, SETD2 is linked to renal cell carcinoma.