In a similar way, in PAH, dynamic and maladapted pulmonary vascular remodeling is accompanied by the acquisition and maintenance of HPASMCs proliferation, migration and secretion of extracellular matrix, growth factors and inflammatory molecules, losing the physiologic quiescent/ contractile phenotype represented by the expression of αSMA and smooth muscle-myosin heavy chain expression. The gene discussed is ACTA1; the disease is pulmonary arterial hypertension.