In COPD patients, the levels of DNA damage markers in lung tissue and peripheral blood cells are increased,408,409 telomeres are shortened,387,410 and the expression of DNA repair-related proteins is decreased,411 all of which are related to disease severity.412 By regulating the expression of telomere protective protein 1 (TPP1), telomerase reverse transcriptase and telomerase (TERC), we can improve cell senescence413 and COPD phenotypes in mice.414 In addition, aging cells release incremental proinflammatory cytokines through SASP reactions, resulting in chronic lung inflammation.415. This evidence concerns the gene POT1 and chronic obstructive pulmonary disease.