Further, a mouse Kir2.1 sequence was used as well as only homomeric mutant Kir2.1 channels, which is not physiologically ideal particularly as ATS is an autosomal dominant disease where WT-mutant subunit interactions may alter channel trafficking and function (8, 10, 11, 12). This evidence concerns the gene KCNJ2 and Andersen-Tawil syndrome.