IL‐17A in lung tissues enhances inflammatory responses by promoting inflammatory monocyte and neutrophil chemotaxis so to clear pathogens effectively.20 However, excessive inflammatory responses may damage tissue.21 Both neutrophils and inflammatory monocytes are involved in pathogen elimination and can cause acute lung inflammation in an IL‐17‐dependent manner.20 In the current study, the data indicates that IL‐17A may not play an important role in driving lung fibrosis at day 28 in mice in response to bleomycin treatment (Figure 1E). This evidence concerns the gene IL17A and pulmonary fibrosis.