Cav3.1 is an emerging target of interest for treating intractable epilepsies, as it has been shown that genetic deletion of Cacna1g, which encodes Cav3.1, reduces spontaneous seizure frequency in a mouse model of Dravet syndrome (Calhoun et al., 2017). This evidence concerns the gene CACNA1G and encephalopathy, progressive, early-onset, with brain edema and/or leukoencephalopathy.