By binding with KEAP1, DPP9 promotes the stability of NRF2 and overcomes oxidative stress, and the accumulation of DPP9 can lead to the hyperactivation of the NRF2 pathway and inhibit ferroptosis, thereby driving ccRCC development and sorafenib resistance (68). This evidence concerns the gene DPP9 and nonpapillary renal cell carcinoma.