Since IFNγ was shown to promote clearance of C. neoformans during clinical trials (Siddiqui et al., 2005; Jarvis et al., 2012) and mice infected with genetically engineered C. neoformans strains expressing IFNγ can clear the infection (Wormley et al., 2007), the diminished IFNγ production could indicate that the activated CD4 T-cells have impaired capacity to completely clear the pulmonary infection, ultimately promoting the persistence of the latent C. neoformans infection in the lungs. This evidence concerns the gene CD4 and infection.