TBCC (tubulin folding cofactor C) is a tubulin-specific chaperone that completes the final step of αβ-tubulin heterodimer assembly 1. Structurally, TBCC functions as a molecular clamp within a cage-like complex with TBCD, TBCE, and the Arl2 GTPase, engaging multiple domains of the αβ-tubulin intradimer interface to promote proper heterodimer maturation 2. This process is essential for microtubule polymerization competency and cytoskeletal proteostasis 1. Clinically, TBCC dysfunction impacts cancer and neurological disorders. In breast cancer, TBCC overexpression reduces polymerizable tubulin pools and microtubule dynamics, leading to G2-M cell cycle arrest, reduced tumor growth, and enhanced chemosensitivity to antimicrotubule agents 3. In ovarian cancer, miR-1251-5p suppresses TBCC expression, promoting cell proliferation and autophagy through altered tubulin and CDK4 levels 4. Additionally, rare damaging variants in TBCC are associated with ADHD, potentially contributing to abnormal late-infancy cerebellar development and immune dysfunction 5. TBCC variants are also implicated in Progressive Encephalopathy with Brain Atrophy and Thin Corpus Callosum (PEBAT), a severe neurodevelopmental disorder featuring neurodegeneration and seizures, with phenotypic severity potentially modified by genetic background 6.