Thus, when Kir2.1 function is impaired, the BMP signaling pathway in iPSC-MSCs is disrupted, diminishing downstream Smad phosphorylation, which is analogous to the diminished Dpp and phospho-Mad signaling seen in dKir mutants in Drosophila. In future studies, it will be interesting to see if the altered bioelectrical patterning defects observed in Xenopus embryos defective for Kir channel function similarly drive BMP secretion defects in mice expressing ATS-causing mutations. This evidence concerns the gene KCNJ2 and Andersen-Tawil syndrome.