Chronic hyperglycemia, hypercholesterolemia, free oxygen radicals, advanced glycation end-products, and protein kinase C are involved in the pathologic process.5 The common characteristic is the increase in levels of vascular endothelial growth factor (VEGF), which is responsible for the disruption of the inner blood–retinal barrier (BRB).6 Disruption of the BRB leads to the accumulation of subretinal and intraretinal fluid, which in turn alters the macular structure and function. This evidence concerns the gene VEGFA and familial hypercholesterolemia.