Considering that TSG6 is responsible for inhibiting monocyte/macrophage recruitment [33], and for converting macrophages from a proinflammatory to an anti-inflammatory phenotype in ALI therapy [34], TSG6 may have presumably mediated the increased therapeutic effect of ITD-pretreated MSCs over IT-pretreated MSCs. The gene discussed is TNFAIP6; the disease is acute respiratory distress syndrome.