The reduction of BMPR2 in human PASMCs, using small interference RNA, and human PASMCs from PAH patients with BMPR2 mutations showed a similar phenotype, with upregulation of pERK1/2 (phosphorylated extracellular signal related kinase 1/2)-pP38-pSMAD2/3 mediating elevation in ARRB2 (β-arrestin2), pAKT inactivation of GSK3-beta, CTNNB1 (β-catenin) nuclear translocation, and reduction in RHOA (Ras homolog family member A) and RAC1 (Ras-related C3 botulinum toxin substrate). The gene discussed is RHOA; the disease is pulmonary arterial hypertension.