The host genetic profile (i.e., genetic polymorphisms) was demonstrated to contribute to the individual predisposition to develop HCC (e.g., variants in gene encoding UDP-glucuronosyltransferase 1A [UGT1A], DNA repair enzymes, glutathione S-transferases, membrane transporters, cytochromes [CYPs]) [6,7] as well as to the prediction of the HCC therapy outcome (e.g., variants in gene encoding drug metabolic enzymes as CYPs and UGT1A1/A9, membrane transporters, vascular endothelial growth factor (VEGF)-dependent and -independent pathways related-proteins) [5]. Here, UGT1A1 is linked to hepatocellular carcinoma.