In summary, TLR-mediated activation of downstream cascades, including NF-κB, MAPK, and MyD88, orchestrates multicellular crosstalk among macrophages, dendritic cells, fibroblasts, and endothelial cells in both hypersensitivity pneumonitis and silicosis, thereby driving coordinated inflammatory and fibrotic responses. The gene discussed is NFKB1; the disease is silicosis.