Given that the tau hyperphosphorylation and accumulation generally resulted from upregulated activity of kinase, such as cyclin-dependent kinase 5 (CDK5) and glycogen synthase kinase-3β (GSK-3β), or downregulated protein phosphatase 2A (PP2A) activity (Iqbal et al., 2009)I, the observed increase of phospho-tau in epilepsy might also be attributed to the dysfunction of these kinase or phosphatases. The gene discussed is GSK3B; the disease is epilepsy.