Because cell junctions, in addition to its adhesive properties, are well-regarded as a cellular structure that blocks tumor growth (39), GIV maintains epithelial integrity (13, 14, 50), we propose a working model (see Fig. 8D) where the two opposing functions of GIV, i.e., tumor suppressor versus oncogene are driven by its subcellular localizations; localization at cell junctions enables GIV-L to exert its tumor-suppressive functions, whereas localization in cytosol enables GIV to access various receptors and G-proteins on basolateral membranes to exert its pro-oncogenic signaling functions. Here, CCDC88A is linked to neoplasm.