Between 2006 and 2007, we reported that Glo2 was differently regulated by estrogens in breast cancer cell lines [156], while it was regulated by the steroid hormone testosterone and estradiol assumable as part of an intracellular response mechanism to the androgen-induced oxidative stress or to the presence of androgen response elements (ARE) in Glo2 promoter, as predicted by bioinformatic analysis [157]. Here, HAGH is linked to breast carcinoma.