ARMC9 is a basal body protein essential for primary cilia formation and function 1. It serves as a scaffolding component of the ciliary tip protein module, working alongside CEP104, CSPP1, TOGARAM1, and CCDC66 to regulate axonemal microtubule dynamics 2. ARMC9 is required for appropriate acetylation and polyglutamylation of ciliary microtubules and regulation of cilium length 1. It functions in hedgehog signaling through regulation of GLI2 and GLI3 proteins at the ciliary tip. ARMC9 physically interacts with the mitochondrial protein NDUFAF2, linking mitochondrial metabolism to cilia signaling; NAD+ supplementation restores ciliary function in ARMC9-deficient cells 3. Mutations in ARMC9 cause Joubert syndrome, a neurodevelopmental ciliopathy characterized by hindbrain malformation and multi-systemic involvement including eye, kidney, and liver pathology 4. ARMC9 variants also associate with vertigo risk through inner ear dysfunction 5. Patient-derived fibroblasts with ARMC9 dysfunction exhibit short cilia with decreased axonemal modifications and aberrant ciliary resorption 1. These findings establish ARMC9 as a critical ciliary protein linking structural organization to human neurological and sensory disorders.