Molecular biology examinations revealed normal levels of CH50 (>70%) and AP50 (>30%), normal activity of ADAMTS13, the absence of anti-factor H antibodies, but a heterozygous variant in exon 22 (SCR20) of the CFH gene (c.3628C>T; p.Arg1210Cys) which was described as the causative mutation for atypical Hemolytic Uremic Syndrome (aHUS). This evidence concerns the gene AP2M1 and atypical hemolytic-uremic syndrome.