Further in vitro study revealed that oxidative stress- and DNA damage-induced senescent BECs exhibited stronger secretion of chemokines (CCL-2/3/4/5, CX3CL-1, CXCL-1, CXCL-2, CXCL-10, and CXCL-16), thereby attracting monocyte/macrophage-like RAW264.7 cells, which suggested that the influence of senescent cholangiocytes on the pathogenesis of PBC was likely achieved by their environmental modulation (116). This evidence concerns the gene CXCL1 and primary biliary cholangitis.