Moreover, a previously unknown role for complement, particularly C5a in ANCA-induced neutrophil activation has been recently suggested.[16,67–70] Interestingly, abnormal cAP activation is also a cardinal feature of TMA, and the hallmark of the aHUS.[13] These defects are either inherited, acquired, or a combination of the two, and they result in chronic, uncontrolled activation of the complement system.[60,71–73] This leads to platelet, leukocyte, and endothelial-cell activation and ultimately to systemic thrombotic microangiopathy.[60,62,63,74–76]. The gene discussed is C5; the disease is Genetic thrombotic microangiopathy.