To further address the mechanistic implications of FTO in Rb1-conferred protection against aberrant endothelial activation in the pathological context of atherosclerosis in vivo, AAV9-mediated overexpression of Fto was targeted to the endothelial cells via a Tie2 promoter and delivered to the HFD-fed Apoe−/− mice in conjunction with Rb1 treatment. The gene discussed is TEK; the disease is atherosclerosis.