In conclusion, IGF2BP3, a non-canonical m6A reader, regulates the abundance of the m6A modification in vitro and in vivo via an effect on glycolysis and OCM, a critical metabolic pathway that significantly impacts cell survival and proliferation, particularly in cancer cells.62 These pathways involve a series of biochemical reactions that fuel the high proliferative and survival demands of cancer cells by supporting nucleotide synthesis and methylation reactions and maintaining redox balance. The gene discussed is IGF2BP3; the disease is cancer.