CNTLN (centlein) is a centrosomal protein required for maintaining centrosome cohesion and proper centrosome function. Structurally, CNTLN localizes to the proximal ends of centrioles where it acts as a molecular linker, directly interacting with both C-Nap1 and Cep68 to form a centrosome cohesion complex 1. Depletion of CNTLN impairs Cep68 recruitment to centrosomes and causes centrosome splitting, demonstrating its essential role in centrosome architecture 1. CNTLN is phosphorylated by Nek2A kinase, suggesting regulatory control of centrosome cohesion during the cell cycle 1. Beyond centrosome function, CNTLN variants show associations with multiple phenotypes. A genome-wide association study identified CNTLN variants (rs10511632) associated with facial morphology, specifically nasal width in a Korean population 2. In cardiovascular studies, rs894379 in CNTLN was associated with increased left ventricular mass in hypertensive individuals 3. Additionally, CNTLN appeared in analyses of gestational age associations and Alzheimer's disease resilience 45, though the mechanistic links between centrosome function and these systemic outcomes remain unclear. CNTLN deletions show marginal association with psychosis in Alzheimer's disease patients 6. These diverse associations suggest CNTLN may have functions beyond centrosome cohesion or that centrosome dysfunction affects broader physiological processes.