Furthermore, in IR-induced or infectious-associated ALI/ARDS, elevated oxidative stress (e.g., ROS) or LPS/TLR4 signaling can increase diacylglycerol (DAG) production, which directly activates endothelial TRPC6, and augmented TRPC6-mediated Ca2+ influx also results in endothelial hyperpermeability and pulmonary edema [109, 117]. The gene discussed is TLR4; the disease is acute respiratory distress syndrome.