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. This evidence concerns the gene NFKB1 and hypersensitivity pneumonitis.