The mechanisms of how highly conserved intraflagellar transport (IFT) protein complexes direct ciliary entry remain unknown. Exploring human ciliopathy genes, including monogenic obesity syndrome genes, has been a rich source of critical ciliary mechanisms. Using AP-MS purification of interactors of the CEP19 monogenic obesity gene, we identify factors and the first known mechanism for triggering ciliary entry of IFT complexes. CEP19 binds the CEP350 and FOP centriolar components and the highly conserved RABL2 GTPase. We discovered that the CEP19-RABL2 complex is first recruited by the centriolar CEP350/FOP complex, concurrently activates nucleotide exchange to capture and release intraflagellar transport B holocomplexes from a large centriolar pool to intraflagellar transport. The CEP19 network of interacting proteins regulates ciliary entry and ciliation, providing a new example of ciliary mechanisms deficient in monogenic obesity syndromes.