Objectives: Invs and DVL-1 expression patterns in the liver of yot (Dab1-/-) mice are the focus of this study, which attempts to clarify their possible roles in the pathophysiology of hepatic abnormalities linked to the Dab1 loss. This study aims to advance knowledge of the molecular processes that underlie the emergence of hepatic dysfunction in the context of Dab1 disruption, elucidating possible ramifications for hepatic physiology and associated treatment approaches. Materials and methods: Homozygous Dab1−/− yot mutant mice, who have an autosomal recessive mutation of the Dab1 gene, and C57BL/6N wild-type mice were used. The gravid mice were sacrificed on embryonic days 13.5 and 15.5 in order to obtain their embryos and their tissue was fixed and stained using immunofluorescence antibodies for Inversin and Dvl-1 proteins. The groups were analysed using a two-way ANOVA test. Results: The findings revealed distinct positive expression patterns, differing in intensity, distribution, and quantity. In wild-type mice, the percentage of Invs-positive cells increased from gestation day E13.5 to E15.5, while it decreased in yot mice over the same period. Specifically, at E13.5, Invs expression was significantly higher in yot mice compared to wild-type mice but dropped significantly by E15.5. In contrast, Dvl-1 expression patterns showed minimal variation between the two phenotypes at both time points, with generally higher percentages of Dvl-1 positive cells in wild-type mice. Over the period from E13.5 to E15.5, wild-type mice exhibited a decreasing trend in Dvl-1 positive cells, whereas yot mice showed an increasing trend. Conclusion: Hematoxylin and Eosin (H&E) staining indicates no significant liver morphology differences between control and yot mutants, while Inversin expression increases in wild-types and decreases in yot mutants from E13.5 to E15.5, with yot mutants showing higher Invs expression at E13.5 but a significant decline by E15.5. Conversely, Dvl-1 positive cells decrease in wild-types and increase in yot mutants, with Invs and Dvl-1 co-expressed in hepatocytes, suggesting interaction in liver development and potential compensatory mechanisms.