Previous studies have shown that rare CFH variants underlying atypical hemolytic uremic syndrome and EOMD can prevent or delay secretion of FH32, 33, 34, 35 or can impair protein function severely, causing reduced FH activity22, 25, 33, 36 leading to dysregulation of the complement pathway. The gene discussed is FH; the disease is atypical hemolytic-uremic syndrome.