Further evidence supporting the role of potassium channels in AF comes from the identification of loss-of-function mutations in the KCNA5 gene, encoding for the Kv1.5 voltage-gated potassium channel responsible for the ultra-rapid component of the delayed rectifier potassium current, in families with hereditary lone AF [69,70]. The gene discussed is KCNA5; the disease is atrial fibrillation.