In addition, in vivo Treg blockade by using nondepleting monoclonal antibodies to CD25, a marker for these cells, diminished the myocardial inflammation in the chronic infection, a finding that was partially ascribed to consequent increased levels of IL-2 secretion and expansion of CD4+CD25+ regulatory T cells (Nihei et al., 2014; Bonney and Engman, 2015), providing an indication that the functional activity of Treg cells might be of critical importance during the chronic phase of the infection. The gene discussed is IL2RA; the disease is infection.