SP-A2 exhibits a significant higher activity of host-defense functions, such as phagocytosis (47, 48, 59) as well as in survival in response to infection (32) compared to SP-A1, whereas SP-A1 exhibits higher efficiency in pulmonary surfactant structural reorganization and in the inhibition of surfactant function by serum proteins (66). The gene discussed is SFTPA1; the disease is infection.