Many previous studies had shown that focal cerebral ischemia can activate m-calpain in the hippocampus, cortex, and striatum through upregulating its protein expression at 1 h after cerebral ischemia [46], and then trigger calpain-mediated STEP (striatal-enriched protein tyrosine phosphatase) lysis and induce neurotoxicity [47]. The gene discussed is CAPN2; the disease is brain ischemia.