Our data thus suggest that it could likely contribute to the initiation of PAH similar to KCNK3 and KCNA5. In line with these findings, in a very recent paper having analyzed 1,038 whole genome sequences from idiopathic and familial PAH, heterozygous mutations at ATP13A3 showing functional impact on protein catalytic activity were observed in 11 patients23. This evidence concerns the gene KCNK3 and pulmonary arterial hypertension.