CNOT7 is a catalytic subunit of the CCR4-NOT deadenylase complex with 3'–5' poly(A) exoribonuclease activity that regulates mRNA stability and translation. The complex mediates bulk mRNA degradation, miRNA-mediated repression, and translational repression during initiation, with function partially redundant with CNOT8 1. CNOT7 associates with BTG family proteins and is required for their anti-proliferative activity. Clinical relevance spans multiple malignancies. In glioma, CNOT7 is highly expressed and correlates with poor prognosis; knockdown inhibits proliferation, migration, and invasion via G2M checkpoint and IL6-JAK-STAT3 pathways 2. In hepatocellular carcinoma, CNOT7 facilitates metastasis by degrading SOCS3 mRNA, sustaining JAK2/STAT3 signaling; antisense oligonucleotide targeting MEX3C–CNOT7 interactions suppressed metastasis 3. In ovarian cancer, CNOT7 promotes proliferation and invasion through the AKT pathway; the AKT inhibitor LY294002 partially reversed CNOT7-driven effects 4. In colorectal cancer, CNOT7 promotes radiotherapy resistance by stabilizing XRCC6 and enhancing DNA repair; combining XRCC6/XRCC5 inhibitor STL127705 with radiotherapy showed promise in patient-derived models 5. CNOT7 also regulates lipid deposition in nonalcoholic fatty liver disease, with knockdown reducing lipid synthesis 6. Recent evidence indicates CNOT7 can induce mRNA degradation from unconventional sites across the mRNA, suggesting broader therapeutic targeting potential 7.