It was reported that inhibition of PDE5 by Sild alleviates symptoms in several cardiopulmonary diseases including PH36 and rescues hypoxia-induced RV hypertrophy.37 This phenotype is the outcome of the increase of cGMP secondary to upregulated eNOS phosphorylation,38, , , , -43 which translates into mitigated apoptosis. The gene discussed is PDE5A; the disease is cor pulmonale.