Because loss of endothelial FTO prevents the progress of obesity-induced hypertension (23), and KLF5 is an essential regulator of angiotensin II signaling-associated cardiovascular remodeling (21), we attempted to elucidate the underlying mechanisms by which both FTO and Klf5-mediated angiotensin II (AngII) induced proliferation and migration of VSMCs. The gene discussed is AGT; the disease is obesity due to melanocortin 4 receptor deficiency.