While SCs were evident within remodeled pulmonary arteries of PAH patients and the experimental PH models, the use of pharmacological and genetic interventions targeting SCs, including activation of a conditional suicide gene driven by the p16 promoter, senolytic drugs (ABT263 and FOXO4-DRI), and inactivation of p16 in transgenic p16LUC/LUC mice, significantly worsened hemodynamic and structural changes (11), suggesting that cellular senescence plays an adaptive, rather than a pathological role, in this disease. The gene discussed is CDKN2A; the disease is pulmonary arterial hypertension.