Complete CFI deficiency is believed to be rare and, as would be predicted, has mainly been reported in association with primary infection (including CNS infection) with encapsulated microorganisms.1 Heterozygote status for CFI deficiency has been associated with atypical hemolytic uraemic syndrome (aHUS) (i.e., not associated with Escherichia coli gastroenteritis)2 and age-related macular degeneration.3 CFI-mediated complement regulation may also be important in the progression of early phase Alzheimer disease.4 This evidence concerns the gene CFI and age-related macular degeneration.