EVI5 (ecotropic viral integration site 5) is a multifunctional regulator with roles in cell cycle control, cytokinesis, and membrane trafficking. It functions as a GTPase-activating protein (GAP) for Rab11 during cytokinesis 1 and stabilizes the APC/C inhibitor Emi1 in S/G2 phase to regulate cell cycle progression 2. EVI5 also interacts with and stabilizes c-Myc protein, antagonizing FBXW7-mediated degradation 3. Genetically, EVI5 represents a significant susceptibility locus for multiple sclerosis (MS). Large-scale genome-wide association studies identified EVI5 as a putative MS susceptibility gene 4, with subsequent Mendelian randomization and co-localization analyses confirming it as a potential therapeutic target for MS 5. EVI5 is also dysregulated in multiple malignancies: it cooperates with BCL6 in lymphomagenesis 6, is upregulated and promotes proliferation, migration, and metastasis in non-small cell lung cancer through the miR-486-5p/TGF-β signaling axis 2, and similarly promotes laryngeal squamous cell carcinoma progression 3. In hepatocellular carcinoma, EVI5 is suppressed by miR-135b, which reduces invasiveness 7. These findings establish EVI5 as both a cell cycle regulator critical for immune function and an oncogenic driver in multiple cancer types.