As previously mentioned, studies on hypoxic–ischemic encephalopathy found that GPR39‐mediated decreases in the expression level of IL‐6, IL‐1β, and TNF‐α promoted the anti‐inflammatory effects of these factors, which could significantly reduce the extent of cerebral ischemia caused by ischemia and hypoxia; moreover, the activation of GPR39 increased the expression level of SIRT1, PGC‐1α, and Nrf2 and reduced the number of neuronal deaths.11 Here, GPR39 is linked to brain ischemia.