Using a conditional knock-out animal model, Schulze-Bergkamen H and his team demonstrated that hepatocyte-specific deletion of Mcl-1 not only increases spontaneous hepatocyte apoptosis resulting in profound liver cell damage and increases susceptibility of hepatocytes to pro-apoptotic stimuli [25], but also, more importantly, triggers hepatocellular proliferation and causes HCC [26]. Here, MCL1 is linked to hepatocellular carcinoma.