FBXO7 (F-box protein 7) is a substrate recognition component of SCF E3 ubiquitin ligase complexes that mediates proteasomal degradation of target proteins 1. The protein functions in multiple cellular processes including cell cycle regulation, mitochondrial quality control, and inflammatory pathway suppression. In mitophagy, FBXO7 operates downstream of PINK1 to target damaged mitochondria for selective autophagy by promoting PRKN relocalization 1. FBXO7 also ubiquitinates multiple substrates including PRMT1 (suppressing serine synthesis in hepatocellular carcinoma) 2, INF2 (inhibiting mitochondrial division in endometrial cancer) 3, and Rbfox2 (controlling alternative splicing in glioblastoma) 4. Additionally, FBXO7 stabilizes Mtus1A through K6-linked ubiquitination, maintaining mitochondrial-ER communication after myocardial infarction 5. Clinically, FBXO7 mutations cause Parkinson disease 15 (PARKIN15), an autosomal recessive form with early disease onset 67. FBXO7 acts as a tumor suppressor in multiple cancer types, with downregulation associated with poor outcomes in hepatocellular carcinoma, endometrial carcinoma, and glioblastoma. The protein represents a potential therapeutic target for both neurodegenerative diseases and cancer treatment 1.