To assess the contribution of ccRCC pathways hypermethylated for m6A in a SETD2 dependent manner to cell growth and viability, we performed cell proliferation and colony formation assays and measured activation of caspase 3/7 with METTL3 depletion in SETD2 WT and KO 786-O cells. This evidence concerns the gene METTL3 and nonpapillary renal cell carcinoma.