Li and colleagues demonstrated that exposure to cigarette smoke extract increased cell senescence and decreased CLOCK and BMAL1 expression in human bronchial epithelial cells, while overexpression of BMAL1 and CLOCK inhibited senescence through the MAPK pathways, suggesting that BMAL1 or CLOCK deficiency may contribute to the development of COPD by promoting cellular senescence in the lung (Li et al., 2022). Here, BMAL1 is linked to chronic obstructive pulmonary disease.