Despite multiple efforts have been made to evaluate the effect of KL on the reverse of hallmarks of aging lung [8], such as cellular senescence [17], mitochondrial dysfunction [16], and stem cells exhaustion [18], the molecular mechanism underlying the protective effect of KL against pulmonary fibrosis remains murky, especially KL’s regulatory role in pulmonary fibroblasts, the effector cells during the development of IPF [19]. The gene discussed is KL; the disease is pulmonary fibrosis.