LGALS3 and neoplasm: Recently, based mostly on prostate cancer experiments, we have proposed the model, whereby adhesive interactions between tumor and endothelial cells initiated by cancer-associated TF-Ag causes translocation and clustering of the endothelium-expressed Gal-3 at the sites of adhesion, which in turn signals mobilization of the α3β1 integrin that strengthens and stabilizes tumor/endothelial cell adhesion [13].