The two FPR antagonists Boc-FLFLF and cyclosporine H are functional in rodents since they significantly reduce monocyte and neutrophil recruitment in murine pneumococcal pneumonia [58],[59] and impair the protective effect of fMLP on infarct size in a rat model of ischemia reperfusion injury [60]. This evidence concerns the gene FPR1 and pneumococcal pneumonia.