CNTRL (centriolin) is a centrosomal protein primarily involved in cytokinesis and cell cycle progression. During late cytokinesis, CNTRL anchors exocyst and SNARE complexes at the midbody, facilitating secretory vesicle-mediated abscission and enabling cell division completion. The protein localizes to centriolar subdistal appendages and functions within the microtubule organizing center. CNTRL has clinical relevance in hematologic malignancies through its involvement in gene fusion events. CNTRL-FGFR1 fusion proteins generate constitutively active kinases that drive myeloproliferative neoplasms 1. These fusions abnormally activate signaling pathways controlling myeloid and lymphoid cell development and differentiation, leading to aggressive myeloid and lymphoid malignancies that progress to acute myeloid leukemia 2. The CNTRL-FGFR1-associated disease is resistant to standard chemotherapy, highlighting the clinical challenge of targeting this fusion event. Beyond hematologic cancers, CNTRL mutations have been identified in dedifferentiated liposarcoma, where CNTRL alterations are associated with worse overall survival 3. Additionally, CNTRL was identified as a switch gene involved in molecular pathways linked to loneliness and associated with neuropsychiatric and neurodegenerative diseases including depression 4. These findings suggest CNTRL functions extend beyond cytokinesis into cancer development and possibly neuropsychiatric disease pathways, making it a potential therapeutic target in malignancies harboring CNTRL fusions.