Complete loss of PML in the HBsAg-transgenic mice (PML−/−HBsAgtg/0) conferred a strong growth advantage and altered lipid metabolism, predisposing the mice to obesity and accelerating the development of multiple hyperplasial foci and large fatty adenomas, which appeared at 12-20 weeks of age, followed by formation of solid adipose-like HCCs by one year of age. This evidence concerns the gene PML and obesity disorder.