According to one study, mice with Atg16l1 and Atg5‐deficient‐PCs presented irregularities in the granule exocytosis pathway, which is observed in CD patients with the homozygous ATG16L1 risk allele (Atg16l1T300A) (Cadwell et al, 2008). This evidence concerns the gene ATG5 and Cowden disease.