It is reported that serum soluble C5b-9 levels are similar to those in plasma when the sample thawed at room temperature.[13] Moreover, elevated levels of C5b-9 have been reported in cases of acquired TTP or sepsis-induced DIC, but not in specific atypical hemolytic uremic syndrome cases.[14–16] However, the elevated level of soluble C5b-9 in our study was much higher than that reported in the case of septic DIC that was accompanied by complement component 3 reduction, indicating complement alternative pathway activation. The gene discussed is C3; the disease is atypical hemolytic-uremic syndrome.