ECs modulate the immune system, impacting immune cell function,[84] and their dysfunction is a mechanism underlying ARDS development.[85] EC necroptosis upon RBC transfusion releases receptor‐interacting protein kinase 3 (RIPK3) and high mobility group box 1 (HMGB1), aggravating lung inflammation via the receptor for advanced glycation end products (RAGE), confirmed by increased RIPK3 levels in patients with transfusion.[53, 54] ECs could be TRALI‐initiating factors. Here, HMGB1 is linked to acute respiratory distress syndrome.