These data, taken together with previous studies demonstrating cell-intrinsic IFN-γ responsiveness by HSC (Baldridge et al., 2010), suggest that IFN-γ may exert its pathogenic role in colitis not only by promoting effector functions in mature leukocytes but also by boosting the hematopoietic activity at the level of the primordial HSCs that sustain the increased production of downstream and non-self-renewing GMPs. The gene discussed is IFNG; the disease is colitis.