Furthermore, although reduced IK,ACh current has been detected in animal models of AF,38,67 downregulation of underlying Kir3.1 and Kir3.4 channel subunits was absent in animal models.39 In contrast, expression of Kir3.4 (KCNJ5), but not Kir3.1 (KCNJ3) mRNA was reduced in aEHM subjected to TP, which is in accordance with findings in AF patients, where protein expression of Kir3.4 is more strongly reduced compared to Kir3.1.34 These data indicate that reduced expression of IK,ACh channels represents a human-specific mechanism in IK,ACh remodelling. The gene discussed is KCNJ3; the disease is atrial fibrillation.