CTNNB1 (beta-catenin), which is degraded through a ubiquitin-dependent mechanism, is stabilized upon activation of the WNT pathway and functions as a transcriptional co-activator of WNT-responsive genes. Some cancers like colorectal cancers develop dominant acting mutations in Ctnnb1 that lead to constitutive WNT signaling and cellular transformation. In this study, originally designed to develop a model of CTNNB1-induced colon cancer, we observed that mice carrying both a conditional stabilizing mutation of the Ctnnb1 gene (Ctnnb1tm1Mmt, hereafter called Ctnnb1F(Ex3)) and a Cre recombinase whose expression is under the control of the murine villin 1 promoter (Tg(Vil-cre)997Gum/J, hereafter called Vil-cre) believed to be specific to the colon and kidney die during embryonic development. To isolate the time point of embryonic death, pregnant dams were euthanized and their embryos dissected at various time points, starting with E10.5. All embryos were inspected for gross abnormalities, and PCR was used to determine the genotype of the embryos. We found that while no double-heterozygous mice were observed neonatally, the litters dissected at E10.5 were developmentally normal and exhibited Mendelian inheritance ratios, suggesting the observed embryonic lethality was not due to preimplantation defects as has been reported for Ctnnb1 null embryos. However, an increase in reabsorption sites was noted at E13.5 and some remaining embryos exhibited delayed development. These abnormal embryos were found to carry both the Ctnnb1F(Ex3) and Vil-cre alleles. These results are suggestive of placental defects. Identifying the molecular mechanisms underlying the cause of embryonic lethality will allow us to better characterize the role of canonical WNT signaling in placental development. Furthermore, the Vil1 gene has been implicated in gut development and is known to be expressed as early as E9, but has yet to be involved in placental development. Ongoing efforts are focusing on the determining the exact cause of embryonic lethality in Ctnnb1F(Ex3)), Vil-cre double mutants.