Depletion of Tregs led to exacerbated cardiac inflammation and dysfunction, whereas expansion of this subtype via super-agonistic anti-CD28 monoclonal antibody 12, interleukin-2 and anti-interleukin-2 antibody complex (IL2C) 13, or adoptive transfer of Tregs 14, 15 contributed to heart healing post-MI 16. The gene discussed is IL2; the disease is myocardial infarction.