Involved in primary cilium biogenesis (PubMed:31761534, PubMed:11062270, PubMed:21289087). Also involved in autophagy since it is required for trafficking of ATG16L and the expansion of the autophagic compartment. Component of the IFT complex B, at least composed of IFT20, IFT22, HSPB11/IFT25, IFT27, IFT46, IFT52, TRAF3IP1/IFT54, IFT57, IFT74, IFT80, IFT81, and IFT88 (PubMed:19253336, PubMed:23810713). Interacts with IFT20, IFT22, HSPB11, IFT27, IFT52, TRAF3IP1, IFT74, IFT80 and IFT81 (PubMed:19253336). Interacts with IFT172 (PubMed:11062270). Interacts with IFT57 (PubMed:11062270, PubMed:19253336, PubMed:23810713). Interacts with IFT46 (PubMed:19253336, PubMed:17312020). Interacts with TTC30B (PubMed:23810713). Interacts with C2CD3 (PubMed:24469809). Interacts with ENTR1 (via N-terminus) (By similarity). Interacts with LRRC56 (By similarity). Interacts with DZIP1 (PubMed:23955340). Colocalizes with ENTR1 and gamma-tubulin at the basal body of primary cilia. Colocalizes with ENTR1 and pericentrin at the centrosome. Testis. Defects in Ift88 are the cause of recessive bilateral polycystic kidney disease (PKD) with collecting duct and tubule ectasia, and a liver lesion involving biliary dysplasia and/or portal fibrosis. Cilia absent or reduced, virtually no cilia of the normal 5 uM mean length (PubMed:21289087). Conditional knockdown in preadipocytes results in loss of cilia. Mutant mice show a significant reduction of gonadal white adipose tissue and total fat mass associated with reduced serum LEP levels (PubMed:31761534). Extended N-terminus.