Studies in complement-deficient mice have shown that mice are protected from renal failure after ischemia/reperfusion (I/R) [31, 32], and that generation of the anaphylatoxin C5a [33] and the membrane attack complex (C5b-C9 or MAC) [32] may contribute to the pathogenesis of ischemic AKI. The gene discussed is C9; the disease is acute kidney injury.