Additionally, beyond its prometastatic role, LGALS3BP secreted by breast cancer cells may function critically as a pro-angiogenic factor through a dual mechanism: the induction of VEGF (Vascular Endothelial Growth actor) expression in human breast cancer cells by activation of the PI3K/Akt pathway, and stimulation of endothelial cell tubulogenesis in a VEGF-independent, galectin-3- dependent manner [18]. This evidence concerns the gene VEGFA and breast carcinoma.