Studies of experimental inflammatory atherosclerosis, which is altered by conditional deletion of Ift88 and thus removal of cilia (Dinsmore and Reiter, 2016), and the ciliopathy polycystic kidney disease (PKD) implicate cilia/ciliary proteins in inflammatory components of pathogenesis (Viau et al., 2018; Zimmerman et al., 2018). This evidence concerns the gene IFT88 and ciliopathy.