For example, Scn1a+/− mice with decreased Cacna1g (Cav3.1) expression showed improved survival and reduced spontaneous seizure frequency, suggesting CACNA1G as a possible genetic modifier and a potential drug target for Dravet syndrome patients [82]. Here, CACNA1G is linked to encephalopathy, progressive, early-onset, with brain edema and/or leukoencephalopathy.