In conclusion, based on the well-documented association between early-life exposure to inflammation and cognitive impairment in adulthood, the current work depicts that hypermethylation-induced deficiency of TGF-β1 further leads to overexpression of KCC2 in the CA1 region of the dorsal hippocampus, which is the important mechanism underlying the adverse effect of neonatal inflammation on hippocampus-dependent memory. The gene discussed is SLC12A5; the disease is Cognitive impairment.