Given the role of inadequate ATG16L1-dependent autophagy in driving ileal inflammation in Crohn’s disease, the genetic association of ATG16L1 polymorphisms with Crohn’s disease, and the unique dysfunction of Paneth cells in patients with Crohn’s disease27, it is plausible to suggest that the reduced availability of VD receptors may have a greater relevance to Crohn’s disease-specific inflammatory processes than ulcerative colitis-specific processes39. Here, ATG16L1 is linked to Crohn disease.