The protein made by the "KCNJ2" gene forms an ion channel that transports potassium ions into muscle cells. This specific channel (the inward rectifier potassium channel Kir2.1) carries a potassium current known as "I"K1 which is responsible for setting the resting membrane potential of muscle cells and is therefore critical for maintaining the normal functions of skeletal and cardiac muscle. Pathogenic mutations in the "KCNJ2" gene alter the usual structure and function of potassium channels or prevent the channels from being inserted correctly into the cell membrane. Many mutations prevent a molecule called PIP2 from binding to the channels and effectively regulating their activity. These changes disrupt the flow of potassium ions, leading to the periodic paralysis and abnormal heart rhythms characteristic of Andersen–Tawil syndrome.