To further explore the role of the FTO‐PGC1α regulatory axis in ccRCC, we performed the PGC‐1α knockdown in FTO stably overexpressing 769‐P cells, and observed that FTO regulation of oxidative stress and cell proliferation could be largely reversed by PGC‐1α knockdown (Figure 5E,F). This evidence concerns the gene FTO and nonpapillary renal cell carcinoma.