Cilia are hair-like structures enriched in receptors and signaling molecules, which play key roles in signal transduction. Notably, olfactory sensory neurons (OSN) cilia harbor all the machinery necessary for odor detection, and thus are indispensable for olfaction. To date, the regulatory pathways involved in controlling cilia formation in OSN remain elusive. Particularly, OSN cilia have properties of motile cilia, akin to those on respiratory and ependymal cells, yet in most vertebrates, OSN cilia lack motility. In our study, we reveal that mammalian and zebrafish OSN express the master regulator of motile ciliogenesis, foxj1. Interestingly, the expression of foxj1 target genes involved in cilia motility are actively repressed in OSN as compared to motile ciliated respiratory cells, explaining their immotility. Next, we investigated the function of foxj1 in cilia formation in zebrafish OSNs. We observed that OSN cilia are lacking in foxj1 mutants. In line with ciliogenesis defects, we identified that foxj1 mutant display aberrant responses to olfactory cues. Altogether, we identified a novel and critical role of foxj1 in OSN cilia formation but not motility. We argue that understanding the regulatory pathways underlying diversity in cilia formation and function is necessary to better understand sensory deficits in patients with ciliary disorders.