Among the most significant pathological processes underlying PAH are disturbances in the endothelin-1-dependent pathways, as well as in the prostacyclin-mediated pathways; decreased bioavailability of nitric oxide; dysfunction of ionic calcium and potassium channels; mitochondrial metabolism disorders; and disturbances in the renin–angiotensin–aldosterone axis; and genetic abnormalities, including mutations in the bone morphogenetic protein receptor type 2 (BMPR 2) gene and epigenetic alterations [32]. The gene discussed is BMPR2; the disease is pulmonary arterial hypertension.