CAPN2 and status epilepticus: This could account for the activation of calpain-2 following stimulation of extrasynaptic NMDA receptors—resulting in the truncation of PTEN and PTPN13—as well as in the autolysis of calpain-2—resulting in the prolonged activation of calpain-2—which has been shown following TBI or status epilepticus [118,120].