These analyses led us to uncover novel mechanisms behind the production of key tumorigenic inflammatory mediators for CCA such as interleukin 6 (IL6) [22, 23], or mediating pro-carcinogenic metabolic reprogramming [24], involving the activation of KRAS-mitogen activated protein kinase (MAPK) signaling, a central event in cholangiocarcinogenesis [25, 26]. The gene discussed is KRAS; the disease is cholangiocarcinoma.