In recent years, transfusion‐related acute lung injury (TRALI) has developed from an almost unknown transfusion reaction to the most common cause of transfusion‐related major morbidities and fatalities. A clinical definition of TRALI was established in 2004, based on acute respiratory distress, non‐cardiogenic lung oedema temporal association with transfusion and hypoxaemia. Histological findings reveal lung oedema, capillary leucostasis and neutrophil extravasation. However, the pathogenesis of TRALI remains controversial. Leucocyte antibodies, present in fresh frozen plasma and platelet concentrates from multiparous donors, and neutrophil priming agents released in stored cellular blood components have been considered to be causative. As neutrophils and endothelial cells are pivotal in the pathogenesis of TRALI, a threshold model was established to try to unify the various reported findings on pathogenesis. This model comprises the priming of neutrophils and/or endothelium by the patient's co‐morbidity, neutrophil and/or endothelial cell activation by the transfused blood component, and the severity of the TRALI reaction.