Individuals with EA1 are heterozygous for a KCNA1 disease-causing mutation, and they have a wild-type and a mutated allele, which may be equally expressed; so, channels composed of wild-type and mutated subunits may be formed, but this heterozygous allele is enough to alter the function of heteromeric channels containing Kv1.1 subunits [7, 8]. Here, KCNA1 is linked to episodic ataxia type 1.