In our experiments, we observed that the expression of SOD1, a key enzyme involved in the neutralization of superoxide anions (Fukai and Ushio-Fukai, 2011), was significantly decreased in mesenteric vessels from HFD-fed mice, thus suggesting that the endothelial dysfunction elicited by HFD could depend also on the reduced ability of vascular tissues to scavenge superoxide anions. The gene discussed is SOD1; the disease is endothelial dysfunction.