This adds to the previously documented inactivation of prostaglandin E2 by UGT2B17-mediated glucuronidation that abrogated the tumor suppressor functions of PGE2 in B-cells and exposed an enzymatic mechanism by which UGT2B17 might influence CLL progression [6]. The gene discussed is UGT2B17; the disease is B-cell chronic lymphocytic leukemia.