Jin et al. suggested that Ac-SDKP alleviated pulmonary fibrosis through decreasing macrophage activation and inflammatory reaction mediated by inhibiting the toll-like receptor 4 (TLR4) and receptor activator of nuclear factor kappa-B ligand (RANKL) signaling pathways in silicotic rats, cultured NR8383 alveolar macrophages, and the RAW 264.7 murine monocyte/macrophage cell line treated by silica [140]. The gene discussed is TLR4; the disease is pulmonary fibrosis.