Another study confirms the critical role of OTULIN-maintained linear ubiquitination homeostasis in protecting against hepatocyte apoptosis and hepatitis, demonstrating that OTULIN deficiency triggers FADD- and RIPK1 kinase activity-dependent apoptosis, which subsequently induces compensatory hepatocyte proliferation and ultimately drives HCC development in mice [118]. The gene discussed is OTULIN; the disease is hepatocellular carcinoma.