Higher p16 expression was found in human COPD lungs compared to normal patients, and when CS induced impaired pulmonary function and augmented emphysema in WT mice, p16 knockout mice exhibited normal pulmonary function with reduced emphysema and increased alveolar progenitor proliferation [149] (Figure 3 and Table 1). The gene discussed is CDKN2A; the disease is chronic obstructive pulmonary disease.