In most cell types, however, hIDO1 is not only expressed constitutively under normal physiological conditions, but the enzyme is strongly induced in response to inflammation and infection stimuli, with IFN-γ being the main inducer [132,133], making IFN-γ-mediated hIDO1 induction and local L-Trp depletion an important factor able to inhibit pathogen growth [134]. The gene discussed is IFNG; the disease is infection.