The epigenetic silencing of Otubain 2 (OTUB2) in OC leads to mitochondrial metabolic reprogramming by destabilizing sorting nexin 29 pseudogene 2 (SNX29P2), resulting in increased hypoxia-inducible factor-1 alpha (HIF-1α) levels and enhanced glycolysis through carbonic anhydrase 9 (CA9), contributing to tumor progression and chemoresistance [26]. Here, CA9 is linked to neoplasm.