The complement system is a set of circulating blood proteins that work together to promote immune and inflammatory responses. Their principal role is to destroy foreign substances like bacteria and viruses. Complement activation may be initiated in several different ways. These are termed classical, alternative or lectin pathways. However, the final product from all activation pathways is the same; the formation of the Membrane Attack Complex (MAC). The trigger for the classical pathway is either IgG or IgM antibody bound to antigen. Biding of antibody to antigen exposes a site on the antibody which is a binding site for the first complement component, C1. C1 is a macromolecular complex of 2 C1q subunits and a tetramer comprising 2C1r and 2C1s subunits. C1, C4, and C2 interact to form the C3 convertase. The cascade continues recruiting C5 to C9 to finally form the cell membrane destroying complex. INCREASED levels of C1 are seen in acute phase response. While DECREASED levels are associated with either hereditary or acquired C1 deficiency. Acquired C1 deficiency is due to cryoglobulinemia, autoimmune disorders, lymphoenia, angioedema, or sever malnutrition.