LKB1/PAR-4 is essential for the earliest polarization steps in C. elegans embryos and Drosophila oocytes. Although LKB1 is sufficient to initiate polarity in a single mammalian intestinal epithelial cell, its necessity in the formation and maintenance of mammalian epithelia remains unclear. To address this, we completely remove LKB1 from mouse embryos by generating maternal/zygotic Lkb1 mutants and find it is dispensable for polarity and epithelia formation in the early embryo. Instead, Lkb1 loss leads to the extrusion of cells from blastocyst epithelia that remain alive and can continue to divide. Chimeric analysis shows that Lkb1 is cell-autonomously required to prevent these extrusions. Furthermore, heterozygous loss of Cdh1 exacerbates the number of extrusions per blastocyst, suggesting LKB1 has a role regulating adherens junctions in order to prevent extrusion in epithelia.