To understand the mechanisms of LTβR-facilitated ICC progression, we next examined whether LTβR agonism indirectly activates other functionally validated liver cancer pathways.3 Increased levels of CAT, c-MYC, and pSTAT3Tyr705 were detected in AKT/NICD/anti-LTβR livers (figure 4E). This evidence concerns the gene AKT1 and intrahepatic cholangiocarcinoma.