STIL (STIL centriolar assembly protein) is an essential regulator of centriole duplication and cell cycle progression. Functionally, STIL acts as a core component of the PLK4-STIL-SAS-6 module, which initiates procentriole formation by directing the loading of structural proteins SASS6 and CPAP to the procentriole base 1. STIL is required for proper onset of centriole assembly and accurate mitotic spindle organization, with long-term silencing decreasing CDK1 activity and affecting cell survival and cell cycle distribution [UniProt]. The protein also functions as a positive regulator of sonic hedgehog signaling and, in complex with PLK4, modulates cytoskeletal rearrangements and directional cell motility. Disease relevance is substantial: mutations in STIL cause primary microcephaly 7 (autosomal recessive), exemplifying how insufficient STIL expression impairs brain development through defective centriole duplication 2. Notably, STIL deregulation exhibits a dual pathological balance—while loss-of-function mutations cause microcephaly, STIL dysregulation is also associated with cancer through chr1 instability and aberrant cell cycle control 2. STIL interacts directly with microcephaly-associated protein RTTN, and naturally occurring microcephaly mutations impair STIL-RTTN binding, blocking centriole assembly 3. This gene exemplifies how disruption of fundamental developmental processes by single genetic lesions has consequences across embryonic development and postnatal tissue homeostasis.