If the insult persists, chronic activation of M2 can directly regulate the development and progression of fibrotic lung diseases through the production of chemokines, tissue inhibitor of metalloproteinases, and fibronectin, as well as the capability of M2 to differentiate into fibrocyte-like cells that express collagen, opposite to their primary anti-inflammatory activity through the release of TGF-β, IL10, and arginase, controlling wound healing and tissue regeneration (Braga et al., 2015; Kishore and Petrek, 2021). This evidence concerns the gene IL10 and lung disorder.