The controversy over the expression of FTO in osteosarcoma essentially stems from its pleiotropy as an m6A demethylase—when FTO targets Wnt pathway-related genes (such as DACT1), high expression promotes tumor progression; when FTO targets AKT/mTOR pathway genes (such as PDK1), low expression activates pro-cancer signals by enhancing m6A modification. Here, FTO is linked to cancer.