Beyond the enzymatic functions of UGTs in glucuronidation, their interactions with other metabolic enzymes, such as those involved in the catabolism of fatty acids and with the glycolytic enzyme pyruvate kinase (PKM2), are another means by which they might influence diverse metabolic pathways involved in cancer biology, with an impact on cancer-cell phenotypes.81,82 These additional functions, which could also involve UGT isoforms produced by alternative splicing, will need to be assessed to comprehensively understand the contribution of UGTs to the oncogenic phenotype. This evidence concerns the gene PKM and cancer.