Considering that β-catenin and its downstream effector cyclin D1 was increased in the tumor-free as well as in the tumor-bearing areas of the intestine after 56Fe radiation, we speculate that one or more of the additional APC-independent mechanisms of β-catenin stabilization discussed above could be involved in 56Fe radiation-induced intestinal tumorigenesis. The gene discussed is CCND1; the disease is neoplasm.