IFNG and Cowden disease: Therefore, this feature suggests that either there is a much increased release of IFN-γ from the inflamed tissues, which would be compatible with the lymphoplasmacytic character of the infiltrate; or it has some degree of impairment of IFN-γ catabolism, which would be compatible with a model of pathogenesis already suggested for human Crohn’s disease (CD), related to lack or diminished functionality of IFN receptors [42], [43].