This finding is in agreement with earlier studies in mouse models: humanized NSG-SGM3 mice, in which human GM-CSF is stably expressed, showed skewed development of human Foxp3+ Tregs (29), and NOD mice, an animal model for type 1 diabetes, showed expansion of mouse Foxp3+ Tregs after treatment with mouse GM-CSF but not with mouse Flt3-L (59). The gene discussed is CSF2; the disease is type 1 diabetes mellitus.