Collectively, these results are in agreement with our previously proposed model whereby tumor/endothelial cell adhesion is initiated by TF-Ag interactions with endothelial Gal-3 causing translocation and clustering of the later at the endothelial cell membrane and followed by the mobilization of α3β1 integrin further strengthening and stabilizing these adhesive interactions [13]. Here, LGALS3 is linked to neoplasm.