Endothelial injury caused by high-dose conditioning regimens and calcineurin/mammalian target of rapamycin (mTOR) inhibitors for GvHD prophylaxis results in elevated levels of proinflammatory cytokines (e.g., IL-2, TNFα), procoagulant factors (e.g., vWF, TF, factor VIIa), and soluble adhesion molecules, which perpetuates the activation of the complement cascade. Here, MTOR is linked to graft versus host disease.