TP53 and neoplasm: Notably, Jiang et al. replaced lysine residues at sites 117,161 and 162 of p53 with arginine residues in tumor cells to construct acetylation-deficient p53 3KR mutant mice, which did not regulate cell cycle and apoptosis like wtp53, but inhibited SLC7A11 expression and induced ferroptosis [76, 80].