Since TGF-β was thought to be a vital antifibrotic MSC-derived factor in the disordered liver environment [58], Wang et al. concluded that BM-MSC-dependent augmentation of TGF-β pathway may be involved in the beneficent effects of BM-MSC in the therapy of PolyI:C-induced PBC and proposed MSC-derived TGF-β and Treg interplay as a potentially new therapeutic approach for the clinical use of MSCs in the therapy of patients with PBC. Here, TGFB1 is linked to primary biliary cholangitis.