Studies have shown that ROS formation can lead to endothelial dysfunction by activating NADPH oxidase and eNOS uncoupling, and NADPH oxidase is the main enzyme in ROS production.7,8-Dihydroxy-3-methyl-isochromanone-4 (XJP-1) can protect (Figure 1)against ox-LDL-induced cytotoxicity and apoptosis by inhibiting ox-LDL-induced ROS production and increasing the production of NO through the PI3K/Akt/eNOS pathway (Fu et al., 2013). This evidence concerns the gene AKT1 and endothelial dysfunction.