Moreover, recently, PNPLA3-TM6SF2-GCKR-MBOAT7 variants combined in a hepatic fat PRS (PRS-HFC) and adjusted for HSD17B13 (PRS-5) were demonstrated as able to predict HCC more efficiently than single variants assessment and that the association between PRS and HCC, mediated by severe fibrosis, was independent from the latter in clinically relevant subgroups and in those without advanced stages fibrosis [69]. This evidence concerns the gene GCKR and hepatocellular carcinoma.