In 2013, following the similarities between TA-TMA and atypical hemolytic uremic syndrome (aHUS), Jodele et al. first suspected the presence of genetic variants in the complement Factor H (CFH) through the identification of deletions in CFH-related genes 3 and 1 (delCFHR3-CFHR1) in 5 out of 6 children with TA-TMA and IgG autoantibodies against FH in three [30]. The gene discussed is FH; the disease is atypical hemolytic-uremic syndrome.