However, it has also been shown that mice deficient in chemokine receptor 5 (CCR5) (Dobaczewski, Xia, Bujak, Gonzalez-Quesada, & Frangogiannis, 2010) exhibited enhanced myocardial inflammation, enhanced matrix metalloproteinase expression, and worsened adverse LV remodeling following reperfused MI, findings which were associated with impaired recruitment of anti-inflammatory CCR5+ foxp3+ regulatory T cells (Tregs). The gene discussed is CCR5; the disease is myocardial infarction.