Further murine infection models also revealed that AMs can utilize other molecular mechanisms, such as arginase-1 expression, phagocytosis of fungal conidia (48, 56), directed migration toward and phagocytosis of bacterial pathogens, and release of IFN-γ (15, 57), to support pathogen clearance from the alveoli, which is eventually performed by recruited neutrophils and bone marrow–derived macrophages (BMDMs). The gene discussed is IFNG; the disease is infection.