In 1999, Austin et al [19] suggested a mechanistic analogy for the KCNN3 polymorphism may be the small polyglutamine number variations in the calcium channel α1a subunit, encoded by CAG expansions in CACNA1A (a calcium channel implicated in FHM1) [8] which are thought to cause Spinocerebellar ataxia type 6 (SCA6) [20] by loss of channel function mechanism [21]. The gene discussed is KCNN3; the disease is spinocerebellar ataxia type 6.