As described previously, tamoxifen-induced activation of Cre-ERT2 leads to the simultaneous activation of the KrasG12D oncogene and loss of the floxed Apc tumor-suppressor gene, constituting a “molecular switch” that drives the development of colonic dysplasia and cancer development that is genetically and histologically similar to KRAS-mutated colorectal cancer in humans [13]. Here, APC is linked to colon dysplasia.