The results showed that the CAF supernatant, but not the CAFPDGFB(KO) supernatant, significantly activated GSK3β and P65 signaling, which could be weakened by PDGF-BB blockade and PDGFR inhibition (Fig. 8C-D), suggesting that CAFs activated the GSK3β and P65 pathways in CCA cells through the secretion of PDGF-BB. Here, GSK3B is linked to cholangiocarcinoma.