Specific rat models which available for study would include those with mutations in the calcium channel SCN5A in mice which is associated with Brugada syndrome (Milan and MacRae, 2005) and mice with human NaV1.5 variant with a mutation in the anesthetic-binding site that produces an incomplete Na+ channel inactivation (F1759A-NaV1.5), who develop spontaneous AF induction (Wan et al., 2016). The gene discussed is SCN5A; the disease is atrial fibrillation.