In non-alcoholic fatty liver disease-related hepatocellular carcinoma (NAFLD-HCC), researchers observed elevated OGT levels in patients with NAFLD-HCC and NAFLD-HCC cell lines and revealed that OGT could regulate lipid metabolism, thereby activating endoplasmic reticulum (ER) stress, and the JUN N-terminal kinase (JNK)/Jun proto-oncogene, AP-1 transcription factor subunit (c-Jun)/activator protein 1 (AP-1), and NF-κB cascades during the development of NAFLD-HCC (Xu et al. 2017); indeed, the latter has been shown to be a cancer-promoting factor in HCC (Han and Roman 2006). The gene discussed is OGT; the disease is metabolic dysfunction-associated steatotic liver disease.