However, the observation of sustained increases in p-tau levels following kainic acid administration being accompanied by only transient increases in GSK-3β activity (Liang et al., 2009) and the lack of effect on hippocampal p-tau by GSK-3β inhibitor pretreatment in the intra-amygdala kainic acid-induced status epilepticus mouse model (Alves et al., 2019) indicate that GSK-3β is not the only kinase responsible for tau phosphorylation following epileptic activity. The gene discussed is MAPT; the disease is status epilepticus.