Indeed, lack of consistent CD-like enteropathy in humanized mice [61] supports the concept that the accelerated disruption of enterocytes secondary to the adaptive CD4+ T cell insult cannot fully explain CD pathogenesis, supporting the notion that an intrinsic defect of the stem cell compartment in subjects at risk of CD is a key element of CD enteropathy [60, 62]. The gene discussed is CD4; the disease is Cowden disease.