Because constant levels of VEGFA signaling maintain the endothelial phenotype and suppress EndoMT in various experimental models [13,16,17,18], we hypothesized that anti-VEGFA or other treatments to block VEGFA signaling could promote EndoMT in CNV, a fibrotic change that would be enhanced by the pro-inflammatory environment of AMD and would render the resulting CNV lesion less dependent on VEGFA for survival [19,20]. This evidence concerns the gene VEGFA and age-related macular degeneration.