Surprisingly, Weiner et al. (77) and Lee et al. (78) found that IL-21R exerted a neuroprotective effect via Janus tyrosine kinase (JAK)/signal transducer and activator of transcription (STAT) signaling pathways and upregulation of caspase-3, and neuronal cell death and infarct volume increased in IL-21R-deficient mice suffered from ischemia compared with the control group. This evidence concerns the gene IL21R and ischemia.