GSK1016790A increases phosphorylation of eNOS and adenosine 3′,5′-monophosphate-activated protein kinase in the aorta and decreases leukocyte adhesion to tumor necrosis factor α-inflamed endothelium, and oral administration of GSK1016790A reduces atherosclerotic plaque formation in ApoE deficient mice with a western-type diet, suggesting that pharmacological activation of TRPV4 may serve as a potential therapeutic approach to treat atherosclerosis (Xu et al., 2016). The gene discussed is TRPV4; the disease is atherosclerosis.