Chambliss and collaborators [63] demonstrated that activating only the membrane actions of ERα is sufficient to confer a cardiovascular protection: both E2 and EDC stimulates endothelial cell proliferation and migration in an ERα and G protein-dependent manner, accelerated reendothelialization after electric injury, and attenuated the development of neointimal hyperplasia following endothelial injury in a context of hypercholesterolemia (Table 1). The gene discussed is ESR1; the disease is familial hypercholesterolemia.