Unlike HypoPP, NormoPP and HyperPP, which are limited to mutations in channels expressed almost exclusively in skeletal muscle, the Kir 2.1, Kir3.4 channel mutations leading to ATS affect multiple tissues, and are associated with a highly variable phenotype of PP, cardiac arrhythmia, and skeletal and craniofacial anomalies [4]. Here, KCNJ5 is linked to Andersen-Tawil syndrome.