CEP192 is a critical centrosomal scaffold protein required for mitotic centrosome maturation and bipolar spindle assembly 1. As a major regulator of pericentriolar material (PCM) recruitment, CEP192 coordinates the assembly of protein complexes necessary for microtubule nucleation 12. During mitosis, CEP192 depletion prevents gamma-tubulin and pericentrin accumulation at centrosomes, resulting in failed spindle assembly despite normal centriole presence 1. Mechanistically, CEP192 functions as a centrosome-specific activating scaffold for Aurora kinase A (AURKA) and PLK1 3. CEP192 cooperates with CEP152 to recruit PLK4 to centrioles, enabling centriole duplication 4. The conserved Spd-2 domain adopts an extended cradle structure that promotes PCM scaffold assembly through PLK1-mediated phosphorylation and oligomerization 5. Clinically, CEP192 mutations cosegregate with cardiac diseases including left ventricular noncompaction and bicuspid aortic valve, acting as genetic modifiers in combination with MIB1 mutations 6. CEP192 degradation by TRIM37 ubiquitination modulates cancer cell sensitivity to PLK4 inhibition, with implications for neuroblastoma and breast cancer treatment 7. CEP192 mutations also associate with male infertility and Mosaic Variegated Aneuploidy 5.