Studies stated that BDNF and its conjugate receptor (i.e., Tropomyosin receptor kinase B or TrkB) are increased in animal models and humans with epilepsy, particularly in temporal and hippocampal areas, and inhibition of BDNF–TrkB signaling and reinforcing the NPY system could be a potential therapeutic strategy for epilepsy (78). The gene discussed is BDNF; the disease is epilepsy.