This is likely mediated by the unchanged C3 fragment deposition observed on RBCs and suggests that, in CAD, where complement activation is initiated via the classical pathway, iptacopan (an inhibitor of the alternative complement pathway and amplification loop) acts primarily by preventing C5 convertase formation and intravascular (MAC‐mediated) hemolysis, with a potentially lesser impact on C3 convertase formation and extravascular (opsonin‐mediated) hemolysis. Here, C3 is linked to cold agglutinin disease.