The abrogation of AD pathology in the 3xTg model backcrossed to the C5 deficient FVB strain (D.A.Morrissette, PhD dissertation, 2009, UCI) as well as the delay in amyloid accumulation in the C5-deficent mice containing the human APP gene under its own promoter [38] supports, though does not prove, a contribution of C5a. The gene discussed is C5; the disease is Alzheimer disease.