FOXG1 and cardiac arrest: It operated through NO‐regulated FOXG1 expression via cGMP pathway and FOXG1‐heightened c‐Myc promoter activity, which could be enhanced by H2S co‐signaling to inhibit PDE5A (i.e., ↑cGMP).[83] For neuroprotection, it was reported that nitrite, an ischemic reservoir of NO and a potent S‐nitrosating agent, ameliorated brain injury after asphyxial cardiac arrest in rats by S‐nitrosylation of brain mitochondria to reduce reperfusion ROS and maintain ATP generation.