IFT88 is a core component of the intraflagellar transport-B (IFT-B) complex essential for primary cilium assembly and homeostasis 1. As a positive regulator of cilium biogenesis, IFT88 facilitates intraciliary transport and maintains ciliary structure across multiple cell types 1. Post-translational UFMylation of IFT88 at lysine 572 by UFL1 protects it from PJA2-mediated ubiquitination and proteasomal degradation, preserving ciliary function 2. Beyond ciliary roles, IFT88 exhibits cilium-independent functions including spindle orientation and actin organization 1. Mechanistically, IFT88 integrates metabolic sensing through asparagine synthetase-dependent glutamine metabolism during nutrient stress 3. In chondrocytes, IFT88 inhibits TRPV4-mediated calcium influx under excessive mechanical stress, protecting cartilage from calcification and intervertebral disc degeneration 4. IFT88 is critical for craniofacial development, with mutations causing cleft lip and palate through disrupted Sonic hedgehog signaling in cranial neural crest-derived mesenchyme 5. Disease relevance spans multiple ciliopathies: IFT88 mutations contribute to orofacial clefting, intervertebral disc degeneration, and osteoarthritis, where reduced expression correlates with cartilage degradation 546. CEP76 dysfunction impairs IFT88-mediated anterograde transport, expanding the spectrum of centrosome-cilium interface disorders 7. Understanding IFT88 regulation offers therapeutic targets for ciliopathies and degenerative diseases.