These mechanisms include consumption of ADAMTS-13 due to on-going cleavage of excessively secreted ULvWF from activated endothelium during sepsis; inhibition of ADAMTS-13 by inflammatory cytokines such as interleukin −6 (IL-6) ; cleavage of ADAMTS-13 by proteases released from neutrophils during inflammatory conditions and last but not the least functional inactivation by coagulation proteinases [11,22]. Here, ADAMTS13 is linked to Sepsis.