Maintaining the role of YAP1 can rejuvenate senescent cells and oppose the appearance of senescence characteristics associated with physiological senescence or accelerated senescence induced by mechanically defective extracellular matrix.[39] Our previous work has revealed that mice overexpressing YAP1 in alveolar epithelial cells can enhance mitochondrial dysfunction, suppress cellular senescence, and alleviate the progression of pulmonary fibrosis.[18] Herein, our findings revealed that the Hippo/YAP1 pathway plays a key role in NPNT inhibition of alveolar epithelial cell senescence. Here, YAP1 is linked to pulmonary fibrosis.