In our study, BIC down-regulated α-SMA in epithelial cells and fibroblasts and up-regulated E-cadherin in both in vivo and in vitro silicosis models, leading to reduced synthesis of ECM components, indicating that inhibition of EMT and FMT processes by BIC could present other modes of action against silicosis, rather than the simple subsequent response of inflammation blockade. This evidence concerns the gene CDH1 and silicosis.