The ATR protein plays an important role in the response to replication stress as a regulator of the DNA damage response (DDR) and controls cell viability. Mutations of ATR in humans lead to, among other pathologies, neurological defects; indicating a yet unknown role for ATR in non-dividing cells. Researchers from the Leibniz Institute on Aging (FLI) in Jena and the Section of Neuroimmunology of Jena University Hospital have shown that ATR deletion in neurons does not affect brain development and formation, but amplifies neuronal activity and increases susceptibility to epilepsy. This study identifies a physiological function of ATR, beyond its DDR role, in regulating neuronal activity.