Mechanistically, well-substantiated work in lung cancer shows that m6A deposited within the 5′UTR of VEGFA enables cap-independent translation through a YTHDC2/eIF4GI–dependent mechanism, boosting VEGF-A production and angiogenesis in vitro and in vivo; genetic and biochemical perturbations in this axis curb neovascularization and tumor growth, establishing causality rather than correlation. The gene discussed is VEGFA; the disease is lung cancer.