With p53 implicated in cell cycle growth arrest, senescence, apoptosis, and tumor suppression [38] and CC10+ secretory club cells significantly enriched in aging and COPD pathogenesis [39], our findings warrant future research into the molecular pathways through which p53 inhibition may lead to an increased CC10+ secretory cell population in the context of cellular senescence, aging, and carcinogenesis. This evidence concerns the gene SCGB1A1 and neoplasm.