This might involve the upregulation of WNT inhibitors (e.g. DKK1 and SFRP1) as observed in metastatic vs. non-metastatic colon cancer patients [6], but also oncogene-mediated increases in GLI function [24, 83] and cell-intrinsic metastatic reprogramming [84]. The gene discussed is GLI1; the disease is malignant colon neoplasm.