Overall, our observations suggested the following mechanism and intervention of anti-CD36–mediated TRALI (Figure 7): interaction between monocytes and TNF-α–activated lung endothelial cells leads to the upregulation of CD36 expression on monocytes, resulting in increased Ab binding, triggering complement activation, ROS generation, and cytokine production, which are all responsible for the severe endothelial dysfunction in TRALI. The gene discussed is CD36; the disease is endothelial dysfunction.