Genetic variants as well as autoantibodies affecting the C-terminal domains of FH impair the simultaneous binding of FH to sialic acid and C3b and are associated with complement-related diseases such as atypical hemolytic uremic syndrome, age-related macular degeneration and C3 glomerulopathy (12, 13). This evidence concerns the gene FH and atypical hemolytic-uremic syndrome.