OGA, a key regulator of O-GlcNAcylation, promotes tumor growth by destabilizing fructose-1,6-bisphosphatase 1 (FBP1), a metabolic enzyme known for its tumor-suppressive properties.91,92 Through the downregulation of miR-503-5p, ADE-derived circCRIM1 facilitates OGA upregulation, leading to decreased FBP1 stability and promoting increased tumor cell glycolysis, proliferation, and metastatic potential in TNBC cells.93 The gene discussed is OGA; the disease is neoplasm.