IFT43 is a core component of the IFT-A (intraflagellar transport complex A) that functions in retrograde ciliary transport along microtubules from the ciliary tip to the base 1. As part of IFT-A, IFT43 is essential for ciliogenesis and regulates the trafficking of G protein-coupled receptors (GPCRs) to primary cilia 2. Recent studies demonstrate that IFT43 physically interacts with the small GTPase Rab23 to facilitate ciliary translocation of the prostaglandin E receptor 4 (EP4), a key step in cAMP-PKA signaling 3. Functionally, IFT43 localizes to the ciliary tip in transfected cells and is critical for maintaining normal cilium length and architecture 2. Mutations in IFT43 cause multiple ciliopathies affecting skeletal and ocular systems. Homozygous IFT43 mutations produce non-syndromic retinal degeneration with shortened photoreceptor cilia and progressive retinal atrophy 2. IFT43 mutations also cause short-rib polydactyly syndrome with abnormal rib bending and disrupted endochondral ossification 1, and cranioectodermal dysplasia characterized by facial dysmorphisms, limb shortening, and renal insufficiency 4. Additionally, IFT43 haploinsufficiency from microdeletion is associated with intellectual disability, cardiac defects, and myopia, accompanied by defective retrograde ciliary transport 5. These findings establish IFT43 as a critical ciliary protein whose dysfunction compromises multiple organ systems dependent on cilia function.