Accumulating evidences suggested that both the club cells and KRT5−/KRT17+ cells are known to play a pro-fibrotic role [18,64,65], and we also found an increased expression of PLA2G3 in club cells and KRT5−/KRT17+ cells of IPF patients as compared to control and healthy individuals, which further supports the same hypothesis. The gene discussed is KRT5; the disease is idiopathic pulmonary fibrosis.