ATP13A3 and pulmonary arterial hypertension: Consistent with the previously reported role of miR-130/301 family on context-dependent endothelial apoptosis [18], and with the paradigm that endothelial apoptosis is a major trigger for the initiation of PAH [39], we now have demonstrated that depletion of ATP13A3 induces miR-130/301 expression and forced miR-130a expression reciprocally decreases ATP13A3 (Figure 3B,E), suggesting a positive feedback loop consistent with promoting endothelial cell apoptosis and PAH.