SCN5A and autosomal dominant cerebellar ataxia: It also facilitates reentrant excitation, VF/VT, and SCA, as shown for the use of class IC antiarrhythmic drugs (potent INa blockers) (Rogers et al., 1989), and in Brugada syndrome (where 20% of patients have an identifiable loss-of-function mutation in SCN5A, the gene that encodes the NaV1.5 α-subunit of the cardiac Na+ channel) (Meregalli et al., 2005).