On the other hand, activation of p53 may antagonize ferroptosis in human colorectal cancer (CRC) cells and fibrosarcoma cells through various mechanisms, such as promoting the localization of dipeptidyl peptidase 4 (DPP4) to the nuclear enzyme-free pool in a transcription-independent manner, increasing the expression of CDKN1A (encoding p21) and favoring the preservation of GSH (Jennis et al., 2016; Xie et al., 2017). This evidence concerns the gene DPP4 and colorectal carcinoma.