FBXO32 (F-box protein 32), also known as atrogin-1, is an E3 ubiquitin ligase component of the SCF complex that regulates protein stability through proteasomal degradation. In skeletal muscle, FBXO32 is a key marker of atrophy, with expression markedly increased during disuse and sepsis-induced muscle wasting 12. FBXO32 functions through substrate ubiquitination; notably, it catalyzes K27-linked polyubiquitination of cyclin D1, enhancing its stability and promoting cell cycle progression 3. Beyond muscle physiology, FBXO32 exhibits oncogenic roles in multiple cancers. In lung adenocarcinoma, FBXO32 overexpression promotes tumor progression by targeting PTEN for proteasomal degradation, activating the PI3K/AKT/mTOR pathway and driving epithelial-mesenchymal transition 4. In pancreatic cancer, FBXO32 enhances protein synthesis by promoting eEF1A1 polyubiquitination, boosting ITGB5 translation and focal adhesion signaling 5. Clinically, high FBXO32 expression correlates with poor prognosis in both lung and pancreatic cancer patients. Conversely, FBXO32 inhibition enhances sensitivity to CDK4/6 inhibitors and FAK inhibitors, suggesting therapeutic potential. These findings reveal FBXO32's dual role as a muscle atrophy regulator and cancer progression driver.