In cholangiocarcinoma, leptin significantly stimulates EMT by provoking cell migration and invasion, impacting multiple levels of EMT promoters (reducing E-cadherin and β-catenin expression in addition to enhancing vimentin and N-cadherin expression) along with the proangiogenic capability of cholangiocarcinoma cells through the microRNA-122/PKM2 axis [156]. Here, VIM is linked to cholangiocarcinoma.