IFT74 is a core component of the intraflagellar transport (IFT) complex B that mediates ciliary protein assembly and trafficking. As part of the IFT74-IFT81 heterodimer, it forms a tubulin-binding module essential for transporting tubulin into cilia and flagella 1. The N-terminal 40 amino acids are particularly critical for tubulin binding, though they are dispensable for IFT subunit interactions 2. IFT74 also functions as an unconventional GTPase-activating protein for RabL2, facilitating IFT initiation at the ciliary base 3. Dysfunction of IFT74 causes diverse ciliopathies reflecting allele-specific severity. Biallelic splice site mutations cause lethal skeletal chondrodysplasia, while exon 2 deletions produce milder skeletal ciliopathy with motile cilia defects 2. IFT74 mutations underlie Bardet-Biedl syndrome, Joubert syndrome, and primary ciliary dyskinesia through impaired cooperation with IFT25-IFT27 4 and disrupted ciliogenesis and ciliary signaling 5. A hypomorphic exon 2 deletion manifests as combined motile and primary ciliopathy with short-rib thoracic dysplasia, demonstrating that tubulin transport demands differ between ciliary types 6. These findings establish IFT74 as essential for ciliogenesis, ciliary maintenance, and proper skeletal and neurological development.