Studies from an animal model carrying one Cav3.2 mutation associated with childhood absence epilepsy suggest that Cav3.2 mutant channels potentiate NMDA-mediated synaptic transmission via increasing local Ca2+ influx at cortical synapses, thus enhancing the susceptibility to absence-like epilepsy (Wang et al., 2015). The gene discussed is CACNA1H; the disease is epilepsy.