In order to gain a better understanding of the molecular mechanisms that are likely to underpin the effects of the ΔN-Bcat mutation on intestinal tumor multiplicity, we monitored expression of the Wnt/β-catenin target genes myc and Ccnd1, which serve as a gatekeeper in Apc-dependent tumor formation (Sansom et al., 2007) and promote cell cycle progression, respectively. This evidence concerns the gene MYC and neoplasm.