Current therapeutic mAbs as well as endogenous low affinity IgG antibodies to cancer cells often recruit the complement component C1qr2s2 with such low avidity that serum C1-inhibitor is able to rapidly inhibit activated C1r and C1s, and in most cases quickly remove the entire C1qr2s2 complex from the antibody-coated cell surface, resulting in only a trace level of C4b-deposition [10-12]. The gene discussed is C4B; the disease is cancer.