Transfusion‐related acute lung injury (TRALI) is a syndrome characterized by acute respiratory distress following the transfusion of blood components. The pathophysiological hallmark of TRALI is an increased pulmonary microvascular permeability. Several reports demonstrate that the majority of TRALI cases are precipitated by the transfusion of donor antibodies directed against HLA (human leukocyte antigens) or HNA (human neutrophil antigens) expressed on the neutrophils’ surface of the recipient. This antibody‐ antigen interaction is thought to directly cause neutrophil activation and release of cytotoxic agents, with subsequent endothelial damage and capillary leak. Recent observations, however, indicate that other cells may also play a significant role in TRALI. This review will introduce several possible mechanisms of TRALI including the involvement of other blood cells and of the pulmonary endothelium.