In light of our observations that subtle genetic exaggeration of β-catenin increased intestinal tumour formation in Apcmin/+ mice without loss-of-heterozygosity of the wild-type Apc allele, and that monoallelic ablation of β-catenin rescued the anterior defect in Apcmin/flox embryos [24,27], we established treatment conditions where G007-LK would only confer partial effects. This evidence concerns the gene APC and intestinal neoplasm.