Treatment of COPD small airway epithelial cells and fibroblasts with BCL<sub>XL</sub>-PROTAC led to their apoptosis through the activation of caspase 3, along with a reduction in senescence markers such as p21<sup>CIP1</sup>, p16<sup>INK4a</sup> and senescence-associated β-galactosidase. The gene discussed is CDKN2A; the disease is chronic obstructive pulmonary disease.