While high levels of sENG have been identified in several human pathological conditions related to dysregulated vascular permeability, endothelial function, and/or angiogenesis (preeclampsia, coronary atherosclerosis, Alzheimer’s disease, hypertension and diabetes) [43,47,48,49], our study showed microglial activation with enhanced NLRP3, an inflammasome marker, around sENG/VEGF-induced dysplastic vessels (Figure 2). The gene discussed is NLRP3; the disease is coronary atherosclerosis.