Given all of these results, we propose a model to explain the formation of this multi-protein HER2 signaling platform at least in some developing HER2-positive tumors: (1) initial upregulation of HER2 expression, (2) HER2 association with Erbin at the basolateral membrane, (3) HER2-mediated disruption of apical/basal polarity, (4) lateral diffusion of NHERF1, Ezrin, PMCA2 and other proteins, which, in turn form novel physical interactions with HER2/Erbin complexes, (5) enhanced HER2 membrane stability and signaling, and (6) tumor progression. The gene discussed is ATP2B2; the disease is neoplasm.