VEGF-A is the primary factor mediating this process, making it a key therapeutic target.521 Additionally, VEGF-B overexpression disrupts the outer blood-retinal barrier and promotes inflammatory angiogenesis by upregulating cell survival factors.522 Notably, patients with wet AMD and polypoidal choroidal vasculopathy exhibit elevated VEGF-B levels, suggesting its involvement in disease progression, particularly after VEGF-A inhibition.523. This evidence concerns the gene VEGFB and wet macular degeneration.