CDKN2A and chronic obstructive pulmonary disease: Issac et al. reported that the expression of p16 was significantly induced in the lung tissue of a mouse model of chronic obstructive pulmonary disease (COPD); however, genetic ablation of p16 could not prevent cellular senescence or alleviate the symptoms of COPD, indicating that p16 alone is dispensable for the development of COPD induced by chronic smoking [41].