BTG2 is an anti-proliferative protein that functions as a tumor suppressor through multiple cellular mechanisms. Structurally, BTG2 mediates its anti-proliferative effects by associating with the CCR4-NOT deadenylase complex, activating mRNA deadenylation in a CNOT6 and CNOT7-dependent manner 1. BTG2 also physically interacts with PRMT1, a protein-arginine methyltransferase, and modulates transcriptional regulation 2. The protein plays critical roles in cell cycle regulation, DNA damage response, and stress-induced growth arrest 3. In disease contexts, BTG2 demonstrates complex roles depending on cell type. In renal podocytes, BTG2 unexpectedly promotes focal segmental glomerulosclerosis through Smad3-dependent podocyte-mesenchymal transition, indicating context-dependent pathogenic functions 4. Conversely, in solid tumors including lung adenocarcinoma and diffuse large B-cell lymphoma, BTG2 functions as a bona fide tumor suppressor—reduced expression correlates with malignant behavior and poor prognosis 56. BTG1 and BTG2 are frequently deleted or mutated in B-cell lymphomas 3. Clinically, BTG2 expression levels serve as independent prognostic factors in lung adenocarcinoma and may predict immunotherapy response 5. Additionally, the PRMT1/BTG2 axis represents a potential therapeutic target for gastric cancer intervention 7.