ATG16L1 and Crohn disease: A threonine 300 to alanine 300 variation in ATG16L1, which has a ∼50% penetrance in European populations but is much less frequently found in African-American populations (∼5%), has been implicated in the development of Crohn’s Disease and an inability of bacteria to be phagocytosed by cells and then disposed of by digestion in autophagic vesicles [38-39].