Concerning deployment of complement therapeutics during experimental sepsis, complement depletion [161], C1 inhibition [162], specific blockade of C5a [118, 163], C5aR1 [164], genetic deficiency in C5 [165], or genetic absence of C6 [166, 167] have been demonstrated to improve sepsis-induced pulmonary inflammation on a morphological and/or functional level. The gene discussed is C5; the disease is Sepsis.