Our observation that ΔN-Bcat expression co-operates functionally with loss-of-function mutations in Apc rather than gain-of-function Kras mutations implies the existence of a minimal threshold level for canonical Wnt/β-catenin signaling to trigger tumor formation (Roose et al., 1999; Samuel et al., 2009; Albuquerque et al., 2010; Buchert et al., 2010; Leedham et al., 2013). This evidence concerns the gene KRAS and neoplasm.