 Information available to date indicates that CCP modules 1–4 is responsible for the cofactor and decay acceleration activities of factor H, whereas self/non-self discrimination occurs predominantly through GAG binding to CCP modules 7 and/or GAG or sialic acid binding to 19–20.Due to the central role that factor H plays in the regulation of complement, there are a number of clinical implications arising from aberrant factor H activity.Overactive factor H may result in reduced complement activity on pathogenic cells - increasing susceptibility to microbial infections.