It was recently found that the oxidation of CDK4 triggers the formation of a reversible intermolecular disulfide bond between Cys135 of CDK4 and Cys7/8 of cyclin D, which inhibits cyclin D-CDK4 activity, consequently reducing cell proliferation in a mouse model of pulmonary hypertension [93]. This evidence concerns the gene CDK4 and pulmonary arterial hypertension.