CPAP (centrosome assembly and centriole elongation protein) is a critical regulator of centriole biogenesis and centrosome function. Mechanistically, CPAP acts as a microtubule polymerase at centriolar microtubule plus ends, working in opposition to CP110 to impose slow processive microtubule growth essential for proper centriole elongation 1. CPAP is required for centriole duplication and interacts directly with the microcephaly-associated protein STIL to regulate procentriole formation 2. It also recruits CEP295 to nascent centrioles during early S phase in a PLK4-dependent manner 3. Diseases associated with CPAP mutations include primary microcephaly (MCPH6) and Seckel syndrome 4. Loss of CPAP in the developing mouse central nervous system causes formation of monopolar spindles in radial glia progenitors, robust apoptosis, cilia loss, and severe cerebellar hypoplasia 4. A naturally occurring MCPH-causing mutation (E1235V) significantly reduces CPAP binding to STIL, impairing procentriole formation 2. These findings establish CPAP as essential for proper neurogenesis and centriole biogenesis, with clinical relevance for neurodevelopmental disorders characterized by microcephaly and impaired centrosome function.