We next tested the hypothesis that loss of Bcl-G may predispose mice to tumor formation by subjecting Bcl-g−/− and WT mice to the CAC model (Fig. 2a), whereby a single injection of the alkylating mutagen azoxymethane (AOM) leads to the sporadic induction of missense mutations in the Ctnb1 gene in colonic epithelial cells, resulting in stabilization of β-catenin and aberrant activation of the Wnt signaling pathway [14, 15]. The gene discussed is BCL2L14; the disease is neoplasm.