Knocking out Sema7A causes miniature excitatory postsynaptic current (mEPSCs), suggesting that Sema7A promotes excitatory inputs.54 In CNS, Sema7A promotes the growth of neurites and neuroinflammation by binding to β1‐Integrin receptor, which activated Ca2+ currents through effects on voltage‐sensitive calcium channels and excitatory NMDA currents in neurons.61, 62 These changes could enhance the glutamate excitability and burst activities in hippocampus, cause hyperexcitability in neurons, and could further lead to the development of the epilepsy. This evidence concerns the gene SEMA7A and epilepsy.