Given that the Fas/FasL pathway plays an important role in neuronal apoptosis during ischemic stroke [2], we speculated that if CRT expression is increased in the brain after ischemia-reperfusion injury (IRI), CRT may bind to FasL and interfere with Fas/FasL complexation, thereby protecting neurons from apoptosis and relieving ischemia-related damage. The gene discussed is FAS; the disease is ischemic stroke.