BIC additionally suppressed the proliferation, migration, and wound healing capabilities of TGF-β1-pretreated NIH-3T3 cells (Fig. 9A-C), similar to the data obtained with NIH-3T3 cells co-cultured with supernatant, suggesting that TGF-β1 secreted by macrophages may serve as a key factor in BIC-mediated suppression of FMT during silicosis. The gene discussed is TGFB1; the disease is silicosis.