As shown in the Figure 1, pulmonary (Figure 1A) fungal burdens were increased in IDO1−/− mice at 96 h, 2, and 10 weeks after infection, whereas significant increases in the liver (Figure 1B) after 10 weeks of infection showed that the lung of both IDO1−/− mice were concomitant with increased levels of pulmonary NO (Figure 1C), considered a potent fungicidal mediator in pulmonary PCM. This evidence concerns the gene IDO1 and infection.