Pulmonary arterial hypertension (PAH) is driven by vasoconstriction, inflammatory cell infiltration, vascular cell migration, proliferation, and apoptosis.1 Molecular mechanisms regulating PAH pathogenesis are multifactorial involving potassium channels, genetic mutations, serotonin imbalances, estradiol changes, and inflammatory alterations among others.2,3. This evidence concerns the gene KCNA3 and pulmonary arterial hypertension.