Although many genes disrupted in PAH tend to be enriched in the endothelium, ATP13A3 mRNA is expressed at similar levels in hPAECs, BOECs, and human pulmonary artery smooth muscle cells.7 Given that pulmonary artery smooth muscle cell proliferation is a hallmark of medial thickening in PAH, future investigations into the impact of ATP13A3 disruption on smooth muscle cell function would be of interest. This evidence concerns the gene ATP13A3 and pulmonary arterial hypertension.