CSF1R and pulmonary fibrosis: Anti‐CSF1R antibody treatment ameliorates radiation‐induced lung fibrosis by selectively depleting profibrotic IMs, which drive myofibroblast activation via arginase‐1 upregulation; while, AMs depletion shows no therapeutic effect, revealing the potential mechanisms by which the CSF1R antibody exerts its effects.[30] These results suggest the profibrotic role of monocyte‐derived macrophages in lung tissue, and the potent capacity of blocking CSF/CSFR signaling in fibrogenesis.