Semi-genetic elimination of senescent cells using ARF-DTR mice, which express the diphtheria toxin receptor under the Arf promoter/enhancer, or p16-3MR mice, which express the herpes simplex virus thymidine kinase under the Ink4a promoter/enhancer, demonstrated that senescence enhanced pulmonary inflammation, thereby exacerbating their pathologies [10–12]. The gene discussed is CDKN2A; the disease is inflammation.