These findings in the posterior eye resemble our observations in the lenses of aged VEGF‐Ahyper mice and demonstrate that both VEGF‐A‐induced age‐related cataract formation and CNV are strongly promoted by NLRP3 inflammasome‐mediated IL‐1β activation, suggesting a shared VEGF‐A‐induced pathomechanism for these distinct aging eye pathologies. The gene discussed is NLRP3; the disease is aging.