In addition, these studies demonstrated that as well as Glo1, Glo2 represents a novel contributor to PCa progression [90] and, more importantly, that Glo1/Glo2 silencing did not alter the behavior of benign cells [90], suggesting that targeting glyoxalases may represent a strategy to selectively inhibit advanced PCa. This evidence concerns the gene GLO1 and posterior cortical atrophy.