Neovascular age-related macular degeneration (nAMD) is a primary global contributor to significant visual impairment among the elderly.1 The development of macular neovascularization (MNV) results from disrupted equilibrium between pro- and antiangiogenic factors, leading to increased synthesis of pro-angiogenic mediators.2 Intravitreal anti-vascular endothelial growth factor (anti-VEGF) therapy has become the backbone of nAMD therapy, though some patients may exhibit treatment resistance, suboptimal response, or develop tachyphylaxis, necessitating repeated injections.3 This evidence concerns the gene VEGFA and wet macular degeneration.