Currently, there is little information about the leptin-induced molecular mechanisms that regulate the growth of cholangiocarcinoma cells; however, evidence from in vitro studies in HuH-28 intrahepatic cholangiocarcinoma cells indicates that leptin promotes cell proliferation and migration, while in in vivo models of cholangiocarcinoma cells, leptin promotes the activation of the STAT3 and ERK1/2 signaling pathways [187]. This evidence concerns the gene STAT3 and cholangiocarcinoma.