IGF2 and neoplasm: Then, IGF2BP2 interacted with m6A-modified myc to activate glycolysis metabolism, promoting CRC cell proliferation.[83] Gao et al first found that lncRNA 91H expression is elevated in CRC, which can interact with m6A reader protein IGF2BP2 to upregulate insulin-like growth factor 2 (IGF2) expression, causing tumor metastasis.[76]