Previous studies showed that fibroblasts originating from COPD patients had an elevated senescence signature as judged by enhanced expression of CDKN1A/P21 and CDKN2A/P16, increased SA-β-galactosidase activity [45,46], reduced proliferation rates [42,46], and higher secreted levels of proteins associated with the SASP [15]. The gene discussed is CDKN2A; the disease is chronic obstructive pulmonary disease.