Although the upregulation of MT1G seemed to have an effect similar to that of ferrostatin-1 by inhibiting ferroptosis in ccRCC cells induced by erastin and sorafenib, MT1G more likely regulated ferroptosis through GSH metabolism and lipid peroxidation rather than modulation of the level of redox-active iron. This evidence concerns the gene MT1G and nonpapillary renal cell carcinoma.