Two independent groups addressed this question by crossing the TGFβRII-flox/flox with CD4-Cre mice, which leads to the disruption of TGF-β signals only in T cells.[9,10] They found that TGF-βRII deficiency in T cells results in the generation of highly pathogenic T cell subsets with overexpressed FasL, perforin, granzymes, and IFN-g, which in turn causes early-onset lethal autoimmunity. The gene discussed is CD4; the disease is Autoimmunity.