Moreover, in lung fibrosis, macrophages characterized by a highly expression of MerTK promoted the production of TGFβ1, which mediated the activation of other fibrotic cells, including fibroblasts, and their capability to overproduce collagen, therefore further and strongly suggesting a profibrotic role of macrophage MerTK [32]. This evidence concerns the gene TGFB1 and pulmonary fibrosis.