During childhood, HCA can be sporadic but is more frequently associated with predisposing factors such as GSD type I and III, anabolic androgenic steroid treatments with or without Fanconi anemia, congenital or surgical portosystemic shunt (CPSS, CPSS), germline mutation of HNF1-α gene, and familial adenomatosis polyposis (Figures 4, 5, and 6) [22, 23]. The gene discussed is HNF1A; the disease is hepatocellular adenoma.