p38MAPK, which is relevant to COPD pathogenesis, plays an essential role in the development of SASP by activating NF-κB [66], which is also responsible for COPD progression by activating proinflammatory genes encoding cytokines and chemokines, such as IL-1b/IL-8/TNF-a, and enhancing oxidative stress [31,67,68]. Here, IL1B is linked to chronic obstructive pulmonary disease.