Hepatitis B virus (HBV) infection is the leading global cause of hepatocellular carcinoma, with over 350 million people being identified as chronic HBV carriers. Insertional mutagenesis from HBV DNA integration into the host genome promotes genomic instability and synergises with cell cycle dysregulation at an epigenetic and post-translational level, leading to hepatocyte transformation.1 In the context of HBV infection, hepatocellular carcinoma can occur at a young age and in the absence of cirrhosis, with the prognostic outlook being fundamentally linked to the quality and duration of HBV DNA suppression.