In addition, because the docking simulation of MCT-2(1–15) and its derivatives to FPR1 or FPR2 well explained the receptor-specific activation mechanisms by those peptides as well as the results of structure–activity relationships, the present findings with structural information of FPR2 and FPR1 are expected to accelerate the development of specific antagonists for not only FPR2 but also FPR1 for the treatment of various inflammatory diseases including the recent epidemic of pneumonia that often causes multiple organ failure. The gene discussed is FPR1; the disease is pneumonia.