Here we demonstrate that IGF1 directly stimulates Kitl/KITLG expression in gastrointestinal smooth muscles, the natural microenvironment for ICC and GIST [8,21,22], in GIST cells and in LX-2 cells derived from hepatic stellate cells [33], the presumed niche for KIT+ hepatic progenitors [54], inflammatory cells [55] and hepatocellular carcinoma [25]. Here, KIT is linked to intrahepatic cholangiocarcinoma.