Brain sodium channelopathies, which include mutations in SCN1A, SCN2A, SCN3A, and some mutations in SCN8A observed in cases of familial human ataxia and in mice models of ataxia and end-plate diseases (these genes encode the channels NaV1.1, NaV1.2, β1-subunit, and NaV1.6 respectively). This evidence concerns the gene SCN3A and cerebellar ataxia.