MYC is a critical target of IGF2BPs in cancers, and its depletion mimics the phenotypes caused by IGF2BP depletion while its overexpression can rescue the effects of IGF2BP depletion.25 Collectively, IGF2BPs elicit oncogenic functions as m6A readers in promoting proliferation, migration, and invasion of cancer cells through post-transcriptionally regulating the stability and also translation of their key target mRNAs (e.g., MYC). Here, MYC is linked to cancer.