Although Nos2-/- mice displayed no phenotype when challenged with oral candidiasis [14], the ability of an iNOS inhibitor to sensitize mice to a low virulence C. albicans mutant [19] and our gene expression data suggested that increased iNOS induction in colonized kidneys could contribute to the increased resistance of Nos3-/- mice to candidemia and their clearance of the acute colonization. The gene discussed is NOS2; the disease is Candidemia.