 In this study, researchers discovered that mitochondrial dysfunction and glycolysis activation are key features of hepatocellular carcinoma, HCC, and that NOP2 plays a critical role in regulating these processes. They found that NOP2 is highly expressed in HCC cells and is associated with poor prognosis. Knocking out NOP2 in combination with the drug seraphonib resulted in significant tumor growth inhibition. The researchers also identified a mechanism whereby NOP2 increases the expression of glycolytic genes such as LDHA, TPI1, PKM2, and EN01. Additionally, they found that MIC-associated zinc finger protein, MAZ, is the main transcription factor responsible for NOP2 expression in HCC. Finally, they demonstrated that targeting the MAZ slash NOP2 slash CMIC signaling pathway could be a potential therapeutic strategy for treating HCC. Yen-Fong Liu and others.