In previously described MP infections, the possible explanations for this correlation include local vasculitis mediated by cytokines and chemokines (IL-6, IL-8, IL-18 and TNF-a), thrombotic vascular occlusion and hypercoagulability induced by MP, which is associated with surface proteins and chemical mediators produced by MP [5, 6] in the absence of a systematic hypercoagulable state. The gene discussed is IL18; the disease is infection.