Four major subgroups of HCA have been identified, defined by: (a) mutations inactivating HNF1A (H-HCA) occurring in 35% of the HCAs; (b) activation of β-catenin by mutations in exon 3 (bHCA), occurring in 15% of the HCAs; (c) inflammatory phenotype (i-HCA) with STAT3 activation, related in 60% of cases to IL6ST somatic mutations inactivating gp130 and more rarely to STAT3 or GNAS mutations, and occurring in 50% of the HCAs; (d) a remaining 10% of unclassified HCAa (U-HCA) [15]. Here, GNAS is linked to hepatocellular adenoma.