Furthermore, a surprising result from Ian Tomlinson’s group also supported the Goldilocks model, in which a novel Apc mutant mouse (Apc1322T) developed severe intestinal polyposis associated with weaker Wnt pathway activation when compared to ApcMin/+ mice (which are predisposed to develop intestinal tumours after loss of heterozygosity results in Apc mutations on both alleles [75,76]. This evidence concerns the gene APC and intestinal neoplasm.