Xenograft-bearing mice received rhIL-2 in order to support survival of adoptively transferred human Tregs,23 as murine IL-2 is less efficient at promoting proliferation of human T cells than rhIL-2, despite cross-reactivity.65 As recent phase 1 trials of in vitro expanded Tregs in GvHD and type 1 diabetes mellitus showed signs of clinical efficacy without supplemental rhIL-2, it is likely that this is a feature of the experimental system and will not be required in clinical trials in Inflammatory bowel disease (IBD).12, 18, 24. The gene discussed is IL2; the disease is graft versus host disease.