C5 and Genetic thrombotic microangiopathy: A breakthrough therapy drug was eculizumab (Ecu), a humanized monoclonal antibody that blocks the cleavage of the final complement protein, C5, into proinflammatory C5a and C5b as well as the formation of C5b-9 responsible for cell lysis, inhibiting complement-mediated thrombotic microangiopathy (TMA) [13,14,15,16].