ENKD1 is a microtubule-binding protein with pleiotropic cellular functions. Structurally, it localizes to centrosomes and centrioles, where it regulates microtubule organization and stability 1. Functionally, ENKD1 promotes astral microtubule stability and facilitates proper mitotic spindle orientation 2, essential for oriented division of basal keratinocytes. ENKD1 is required for both primary and motile cilia assembly by competing with CEP97 for CCP110 binding, thereby promoting their removal from the mother centriole and initiating ciliogenesis 3. Beyond structural roles, ENKD1 functions as a critical immune regulator. It suppresses innate immune activation by modulating geranylgeranyl pyrophosphate synthase activity and RAC1 signaling 4, and attenuates antibacterial immunity by facilitating TRIM21-mediated degradation of RUBCN to suppress LC3-associated phagocytosis 5. Post-translationally, HDAC6-mediated deacetylation of ENKD1 at lysine 98 impairs its γ-tubulin interaction and centrosomal localization, disrupting mitotic spindle orientation in corneal epithelial cells 6. Clinically, ENKD1 dysregulation correlates with disease pathogenesis. Upregulation promotes diffuse large B cell lymphoma development through disruption of cellular homeostasis 7, while downregulation characterizes non-small cell lung cancer progression 8. In septic acute kidney injury, elevated ENKD1 promotes pathology; conversely, miR-760-mediated ENKD1 suppression ameliorates injury 9. ENKD1 has been identified in novel T-ALL gene fusions 10, suggesting broader oncogenic involvement.