Conceivably, in addition to exacerbated T effector cell activation due to reduced numbers of functional Treg cells, autoimmune disease in Dicerlox/lox × BAC-Foxp3Cre-GFP mice is likely to be driven by self-reactive, initially normal but unstable Treg cells that, as a consequence of Dicer deletion, dedifferentiate into autoimmune T effector cells, overwhelming the population of functional Foxp3+GFP? Treg cells that reside in the periphery. The gene discussed is FOXP3; the disease is autoimmune disease.