Collectively, these findings indicate that METTL3-mediated m6A modifications enhance EC angiogenic behaviors by targeting MMP2 and TIE2, underscoring the importance of the METTL3-MMP2 and METTL3-TIE2 axes in retinal angiogenesis and positioning METTL3 as a potential therapeutic target for oxygen-induced retinopathy. The gene discussed is MMP2; the disease is retinal disorder.