Because the β4 subunit is the primary partner of CaV2.1 in cerebellum and loss‐of‐function mutations of both calcium channel subunits result in ataxia (Burgess et al., 1997; Burgess & Noebels, 1999a; Escayg et al., 2000; Guida et al., 2001; Pietrobon, 2002; Buraei & Yang, 2010; Schlick et al., 2010), it is reasonable to expect that loss of either one of these proteins affects the same brain functions. Here, CACNA1A is linked to cerebellar ataxia.