METTL3/m6A/YTHDF2 mediated degradation of PGC-1α, as well as cytochrome c (CYCS) and NADH ubiquinone oxidoreductase subunit C2 (NDUFC2), inducing mitochondrial dysfunction and oxLDL-induced inflammation in monocytes.340 During myoblasts differentiation, FTO positively modulates mTOR-PGC-1α pathway-mediated mitochondria biogenesis depending on its m6A demethylase activity.32 Consistently, ectopic expression of FTO in VHL-deficient ccRCC cells upregulated expression of PGC-1α to regain mitochondrial activity, exhibiting anti-proliferation effect.341. This evidence concerns the gene METTL3 and nonpapillary renal cell carcinoma.