In vivo studies also demonstrated that rapamycin treatment could enhance TGFβ-dependent FOXP3 expression and generate large-scale human regulatory T cells that suppress disease in a xenogeneic model of GVHD, thus opening the door for using Tregs as a cellular therapy to prevent GVHD, graft rejection and autoimmunity [43]. The gene discussed is TGFB1; the disease is graft versus host disease.