This finding, along with previous observations showing elevated levels of miR-155 in infected Il10-/- joint tissue [21], and STAT3-dependent miR-155 suppression by IL-10 [22], led to the prediction that the IL-10/miR-155 regulatory circuit described by McCoy, et al. [22] might be an important mechanism of immune regulation during Lyme borreliosis. The gene discussed is IL10; the disease is Lyme disease.