reported that Sap1,2,3, mainly Sap2, degrade C3b, C4, and C5 of the complement system, thereby inhibiting complement activation.[9c] Additionally, other studies have found that Sap2 can degrade extracellular matrix (ECM) components to breach physical barriers, aiding in the spread of infection,[13] and mediate the adherence to and invasion of endothelial cells by pathogenic C. albicans. The gene discussed is C3; the disease is infection.