Since our preliminary data suggested VIP was an endogenous modulator of hippocampal CA1 TBS-induced LTP [1], we investigated the cellular mechanisms and hippocampal receptors mediating these effects that may constitute important pharmacological targets to modulate hippocampal-dependent memory processes in pathological conditions like epilepsy, aging or neurodevelopmental disorders [43,44]. The gene discussed is VIP; the disease is neurodevelopmental disorder.