Interestingly, GLI3 has been reported to repress KIT mRNA levels in ICC-like cells of the murine ureter [20], raising the possibility that GLI3 may contribute to the formation of a KITlow/− GIST cell pool [4] responsible, in part, for disease persistence during imatinib therapy [3]. The gene discussed is KIT; the disease is intrahepatic cholangiocarcinoma.