NINL (ninein like) encodes a centrosomal protein essential for microtubule organization and intracellular transport. The protein functions as a dynein activating adaptor that associates with cytoplasmic dynein 1 motor complex subunits, facilitating minus-end directed vesicle transport 1. NINL works in conjunction with DZANK1 to ensure proper assembly and folding of the dynein motor complex, which is critical for photoreceptor outer segment formation and maintenance 1. The protein also interacts with CC2D2A at ciliary transition zones, controlling RAB8-MICAL3-regulated vesicle trafficking and protein entry into cilia 2. Beyond its structural roles, NINL has emerged as an important component of antiviral innate immunity, with knockout cells showing impaired interferon responses and increased viral permissiveness 3. Notably, NINL has evolved under positive selection pressure, particularly in its cargo-binding region, suggesting ongoing host-pathogen evolutionary conflicts 3. Recent studies identify NINL as a modulator of tau aggregation, where overexpression reduces tau seeding and enhances lysosomal proteolytic activity, positioning it as a potential therapeutic target for tauopathies including frontotemporal dementia and Alzheimer's disease 4.