An in silico investigation of the familial AF V93I-Kir2.1 mutation to IK1 by Kharche et al. [17] showed that both heterozygous and homozygous forms of the mutation (which increased both inward and outward IK1) shortened APD, hyperpolarised RMP, flattened restitution curves of APD, ERP, and CV, and stabilised rotors in the 3D virtual human atria. The gene discussed is KCNJ2; the disease is atrial fibrillation.