We dare to speculate that S100A9-dominant classical monocytes might perpetuate tissue damage from lung injury in IPF as precursors of S100A9+ macrophages on alveolar spaces, while CD163-dominant monocytes rather play a protective role with reversibility against lung injury in iNSIP, but not profibrosis that is classically characterized as a major role of M2 polarized macrophages. This evidence concerns the gene CD163 and idiopathic pulmonary fibrosis.