In view of the fact that glutathionylation, as a posttranslational modification, can affect the activity of many proteins involved in tumor growth, while the deglutathionylation process also may expose vulnerable thiol groups in prostate tissue to oxidation, the role of GSTO1 and GSTO2 allelic variants exhibiting altered activities could provide a plausible mechanism to explain the associations between these genetic polymorphisms and risk for PC development. Here, GSTO1 is linked to neoplasm.