These diseases can arise from disruptions in the cilia’s structure, as seen with the loss of IFT proteins [8], and from disruptions in the cilia’s function, for example, due to an altered ciliary protein composition, as seen with mutations of the genes associated with Bardet–Biedl syndrome (BBS) [8] that perturb the normal ciliary localisation of GPCRs, including SSTR3, MCHR1, and NPY2R [6,20]. This evidence concerns the gene SSTR3 and Bardet-Biedl syndrome.