Given the endothelial-protective, anti-fibrotic, and immunomodulatory effects of HDL/apo A-I on the one hand, and the occurrence of vascular inflammation and fibrosis, and innate immune activation under obese conditions on the other hand, we aimed to investigate whether human apo A-I gene transfer can decrease aortic inflammation and fibrosis in leptin-deficient ob/ob mice, which are overweight [32], insulin-resistant [33], and develop vascular inflammation and fibrosis [34, 35]. The gene discussed is LEP; the disease is inflammatory response.