“…(Gooley et al , ; D’Souza et al , ) Despite these advances, several complex post‐HCT toxicity syndromes that share areas of overlapping pathobiology involving endothelial injury and often underlying allogeneic‐mediated reactivity continue to contribute considerable morbidity and risk of mortality. (Cooke et al , ; Carreras & Diaz‐Ricart, ; Panoskaltsis‐Mortari et al , ; Dalle & Giralt, ; Cornell et al , ; Rodrigues‐Diez et al , ; Moiseev et al , ; Pagliuca et al , ) In the modern era, perhaps the most illustrative of these syndromes is transplant‐associated thrombotic microangiopathy (TA‐TMA), a potentially devastating complication resulting from multifactorial endothelial damage and subsequent complement activation leading to microangiopathic haemolysis, microvascular thrombosis, and eventually end‐organ damage. (Laskin et al , ; Jodele et al , ; Postalcioglu et al , ; Dvorak et al , ) Recent evidence suggests that the mechanistic link between endothelial damage and subsequent complement activation may be the formation of neutrophil extracellular traps that activate the classical and alternative complement pathways further propagating of microvascular injury.…”