Consistently, upon BIC-mediated down-regulation of phosphorylated JAK2 and STAT3 in silicosis rat lung and NIH-3T3 cells via suppression of TGF-β1 secretion, ECM deposition was markedly decreased in both tissues and cultured cells, indicating that fibroblast activation and FMT via TGF-β1/JAK2/STAT3 signaling may serve as another mechanism by which BIC targets TGF-β1 to exert therapeutic effects against silicosis. The gene discussed is STAT3; the disease is silicosis.