Decreased current amplitudes, reduced window currents, increased recovery rate, and depolarizing shifts in the voltage-dependence of Kv1.1 will, altogether, more than likely result in an increase in neuronal excitability that in EA1 would manifest as ataxic attacks and myokymia, as observed in the proband and family members carrying the mutation. Here, KCNA1 is linked to Myokymia.