Its dominant role of inward rectification for the normal function of skeletal and cardiac muscles is shown by the complete loss of inward rectifying current and K+-induced dilations in arterial myocytes from Kir2.1 knockout mice [2] and periodic paralysis, and by cardiac arrhythmias in Anderson's syndrome caused by point mutation of human Kir2.1 [3]. This evidence concerns the gene KCNJ2 and periodic paralysis.