Proposed mechanistic link between endothelial injury, complement activation, and TA-TMA and GVHD. Based on our results, our proposed mechanism is as follows: 1. Chemotherapy, radiation, and infection lead to endothelial injury during early stages of HSCT. 2. Endothelial injury releases IL-8, causing neutrophil activation with release of NETs. 3. NET formation leads to complement activation with deposition of complement factor P and C5b-9 deposition. 4. Complement activation results in microthrombi formation. 5. Treatment with complement blockade leads to clearance of NETs and resolution of TA-TMA, but in patients with GVHD, NETs remain secondary to persistent endothelial injury. CFP, complement factor P.