On the other hand, in an experimentally induced rhesus macaque model of CeD, several tight junctions and their associated proteins, such as zonulin and haptoglobin-2, known to also be expressed in the human blood–brain barrier, were shown to be dysregulated, along with the peroxisome proliferator activated receptor gamma (PPARγ) gene, leading to intestinal inflammation, increased permeability, and dysbiosis [21]. The gene discussed is PPARG; the disease is cranioectodermal dysplasia.