This is consistent with the studies performed in APP23 transgenic animal models of AD, where β3 positive vessels were increased in disease susceptible regions [43], and also with studies linking AD to inflammatory mediators (TNFα, IL1β, IL-6, and IL-8), all of them with proangiogenic properties [44, 45], and with in vitro studies showing that microvessels of AD brains release angiogenic mediators such as angiopoietin-2 and vascular endothelial growth factor (VEGF) [46]. The gene discussed is VEGFA; the disease is Alzheimer disease.