Dab1 protein (Disabled-1) is an intracellular reelin signaling pathway adapter involved in prenatal neuronal migration, neurotransmission, memory formation, and synaptic plasticity. Yotari is an autosomal recessive mutant of the mouse Dab1 gene, phenotypically characterized by unstable gait, tremor, and premature death. Previous research has been mainly related to neurological abnormalities caused by the Dab1 mutation, and the role of the reelin signaling pathway in tissues and organs outside the nervous system has not been investigated. Hepatocytes, the most numerous liver cells, communicate through gap junctions (GJs) composed of connexins. In this study, a disorder in cellular communication in yotari mice was investigated by analyzing the expression of connexins (Cxs) Cx26, Cx32, Cx37, Cx40, Cx43 and Cx45 during embryonic day E13.5 and E15.5. Immunofluorescent method was used, analysis was performed on a light and fluorescence microscope, and the result was quantified as the surface of the field of view covered with a positive signal. Data were expressed as mean ± SD (standard deviation) using a one-way ANOVA test. All tested connexins were significantly less pronounced in the yotari mice compared to the control wt mice in E13.5. The expression of analysed connexins in E15.5 is similar, with the exception of Cx37 which in wt mouse shows very slight expression. Channel formation under pathological conditions and propensity to apoptosis were investigated by analysis of the expression of Panexin 1 (Panx1), AIF and caspase 3 during these embryonic periods. The increase in Panx1 expression in E15.5 in the yotari mice, and the higher expression of AIF in both periods possibly indicate that yotari are more prone to apoptosis. Our results highlight the importance of intercellular communication (GJIC) during liver development and their possible role as potential diagnostic markers in liver disease.