An imbalance between the populations of M1 and M2 macrophages is believed to trigger the onset and facilitate the progression of sepsis.[9] During the acute phase of sepsis, M1 macrophages predominate and release significant amounts of proinflammatory mediators, leading to tissue damage.[9] Recent studies have also shown differences in TSPO expression between human M1 and M2 macrophages.[10] However, although changes in TSPO expression have been implicated in sepsis, the potential utility of measuring the plasma TSPO concentrations of patients with sepsis has not been evaluated. The gene discussed is TSPO; the disease is Sepsis.