Third, blocking TRPV4 has been proven to have protective effects on neurons following oxygen-glucose deprivation treatment or in rodent models of acute cerebral ischemia.6, 7, 9, 10, 11 Cell apoptosis is one of the major causes of cerebral ischemic injury, and it may be mediated through MAPK signaling pathways.14 The present study showed that application of a TRPV4 antagonist reduced brain infarction and apoptosis at 48 h post MCAO (Figure 4), indicating that TRPV4-induced apoptosis is likely involved in the cerebral ischemic injury. The gene discussed is TRPV4; the disease is brain infarction.