We observed neuronal loss and gliosis in this cohort, consistent with the hallmarks of epilepsy in humans reported in the literature.79,80 In addition, NR2B-PSD95 interaction was markedly increased in the cortex of the human epileptic brain, which also complements previously reported studies.81-83 Similar to the findings in our animal models, the degree of Fyn-tau interactions positively correlated with NR2B-PSD95 complexes and tau phosphorylation, and activated Fyn levels in human epileptic brain. The gene discussed is DLG4; the disease is epilepsy.