Hepatocellular adenomas (HCAs) are composed of four molecular subgroups: mutations inactivating the HNF1A gene; the inflammatory phenotype with mutations of different genes leading to STAT3 activation; the activation of β-catenin by mutations in exon 3; among β-HCA, half display both inflammatory and β-catenin-activated phenotypes; and the unclassified tumors. The identification of these subtypes by MRI and immunohistochemistry on tissue is considered as a major criterion to manage patients. Of particular relevance is the identification of the β-catenin-mutated group due to its high risk of malignant transformation. In spite of this progress, the classification has not gained recognition among surgeons. It is hoped that by working as a multidisciplinary team, including surgeons, radiologists, pathologists and molecular biologists, patients will be managed more rationally. In this article, we will present known and new data, well accepted and that which is still controversial. The progress made in the field of HCA in the last 12 years, whether in epidemiology, diagnosis (clinical, pathology, imaging) or management, is related in one way or another to molecular advances.