Autoimmune hemolytic anemia (AIHA) is a group of rare autoimmune disorders characterized by the premature destruction (hemolysis) of red blood cells (RBCs) by autoantibodies at a rate faster than they can be replaced.1 Most cases of AIHA are classified as either warm antibody (wAIHA, 60% to 70% of cases) or cold agglutinin disease (CAD, 20% to 25% of cases), depending upon the temperature at which the autoantibodies show maximum binding.2 In wAIHA, IgG antibodies improperly bind to self-proteins on the surface of red blood cells, activating the classical complement pathway, which causes C3b to attach to the cell surface, resulting in extravascular hemolysis, the destruction of red blood cells in the liver and spleen. In CAD, IgM antibodies improperly bind to self-proteins on the surface of red blood cells, causing them to clump together, strongly activating the classical complement pathway which leads to the accumulation of C3b on the cell surface, resulting in extravascular hemolysis. In severe CAD, C3b activates the whole complement cascade, causing the formation of membrane attack complexes, known as MACs, which form holes in the surface of red blood cells, resulting in hemolysis inside blood vessels, called intravascular hemolysis. Learn more about the role of the complement system and C3 inhibition in wAIHA & CAD by watching the video and at https://aihaclinicaltrial.com/ 1) Anemia, hemolytic, acquired autoimmune. National Organization for Rare Disorders Web site. https://rarediseases.org/rare-diseases/anemia-hemolytic-acquired-autoimmune/. Accessed March 1, 2018. 2) Barcellini W. New insights in the pathogenesis of autoimmune hemolytic anemia. Transfus Med Hemother. 2015;42(5):287-293.