Wnts have diverse roles in governing cell fate, proliferation, migration, and polarity during development, particularly in embryogenesis and carcinogenesis in adults1-3. Wnts are transduced through at least three distinct intracellular signaling pathways, including the canonical Wnt/b-catenin, Wnt/Ca2+ and Wnt polarity (also called ‘planar polarity’)2, 4,5 pathways. Distinct sets of Wnt and Frizzled ligand-receptor pairs activate each of these pathways and lead to unique cellular responses. The Wnt/b-catenin pathway primarily regulates cell fate determination during development, whereas the main function of the Wnt polarity pathway is the regulation of cytoskeletal organization. Wnt2B/Wnt13 is expressed in the embryonic mesoderm during gastrulation, and in the dorsal midline of the diencephalons and mesencephalon, the heart primordial, the lung bud periphery, and in the otic and optic vesicles at later stages.6 Wnt2B is expressed in organs regulated by epithelial-mesenchymal interactions in the mouse embryo, such as the developing kidney, lung, salivary gland, gut, pancreas, adrenal gland, genital tubercle, eye and ear.7 Wnt2B signaling induces ureter branching during early kidney organogenesis.7 Wnt2B exists as 2 alternatively spliced isoforms (Wnt2B1 and Wnt2B2).8 Wnt2B2 is preferentially expressed in NT2 cells, with the potential of neuronal differentiation.9 In some cases of gastric cancer, Wnt2B2 up-regulation may lead to carcinogenesis through the activation of the b-catenin/TCF signaling pathway.9 Wnt2B is expressed in the immature ovary, where the Wnt signaling cascade may be involved in follicular development and ovarian function.10