More importantly, we showed that in vivo silencing of Gal-1 expression by tumor cells does not interfere with other pro- or anti-angiogenic factors such as VEGF or thrombospondin and bFGF, revealing the preponderant role of Gal-1 in promoting PCa neovascularization and suggesting Gal-1 as a new potent target for clinic therapeutic approaches in advanced PCa patients [23]. This evidence concerns the gene FGF2 and posterior cortical atrophy.