The important classes of metabolic pathways modified in UGT2B17 KO are elevated ceramides, kynurenine and triacylglycerol, all associated with adverse PCa outcomes [47, 65, 66], whereas more broadly reduced metabolites are observed in UGT2B28 KO, including oxylipins and other inflammatory mediators but with an increase in ceramides/sphingolipids precursors, also linked to PCa cancer growth and invasion/metastasis [48, 49]. The gene discussed is UGT2B28; the disease is posterior cortical atrophy.