Endometrial remodeling is a unique sequence of factors that make it receptive to implantation. Despite extensive research on several molecular components that characterize endometrial receptivity, implantation failures occur in assisted reproductive technology (ART). Therefore, implantation failure remains the “final frontier” of infertility. The great interest is explained by the desire to find out the etiology of implantation failure. The endometrium undergoes changes to regulate paracellular permeability across the epithelium. These transformations are associated with and regulated by associated junctional protein complexes. These multiple factors of tight junctions (TJ), adherent junctions (AJ), and gap junctions (GJ) control communication between the endometrium during implantation, highlighting how molecular architectures and interactions can regulate receptivity. In our previous study, we quantified the expression of zona occludin-1 (ZO-1), E-cadherin (E-cad), claudin-1 (Cla-1), and vascular angiogenic precursor (VAP) by immunohistochemical (IHC) staining. An overview of the current knowledge of protein expression in the endometrium during the pretreatment implantation window is provided. It then explains how protein molecules or cell-cell compounds help counteract endometrial events. A deeper understanding of the connecting molecules will be the basis for new strategies that advance implantation.