The metabolite profiling after incubation with a panel of supersomes overexpressing specific UGT isoforms, correlation with glucuronidation rates of known UGT1A1 substrates using human liver microsomes, and analysis of the mass spectrometry profile of belinostat in a cohort of patients with liver cancer provided evidence that belinostat glucuronidation in vitro and in vivo is mediated primarily by UGT1A1. This evidence concerns the gene UGT1A1 and liver cancer.