The Lrig1-CreERT2/+;Apcfl/+ mouse model of CRC is notable for its high penetrance and rapid onset after the loss of just a single copy of Apc. The extremely high tumor burden observed in Lrig1-CreERT2/+;Apcfl/+ mice is especially striking considering that prior to the spontaneous loss of an Apc allele, tamoxifen-induced Cre-recombination of the other Apc allele, must first occur in the same cell under the control of the Lrig1 promoter, which is also a rare event. Here, APC is linked to colorectal carcinoma.