SLC12A5 and status epilepticus: In vivo, knock-in mice expressing homozygous phosphomimetic KCC2 mutations at T906/T1007 die early postnatally [14,15]; in mice with constitutive dephosphorylation of T906/T1007, the onset of seizures is delayed and the severity of seizures attenuated [16], whereas in mice harboring the S940 mutation, both the development and lethality of status epilepticus is accelerated [17].