The disease is associated with heterozygous variants in genes encoding complement proteins and regulators including complement factor H, factor I, membrane cofactor protein, (CD46), C3, factor B, and hybrid genes or deletions in factor H-related proteins, or autoantibodies to factor H, leading to uncontrolled alternative complement pathway activation on endothelial cells and thrombotic microangiopathy.2 The gene discussed is CD46; the disease is thrombotic microangiopathy.