Given that ovarian cancer sustains the highest frequency of TP53 gene mutation which leads to the downregulation of FBW7 [6, 7, 21], our study indicates a potential interplay between mutant p53 and the FBW7-YTHDF2 axis, and suggests an alternative working model for the “gain-of-function” of mutant p53 through the regulation of m6A-dependent RNA turnover [48]. The gene discussed is TP53; the disease is ovarian carcinoma.