In support of this hypothesis, ex vivo transcriptional studies from malaria-naïve individuals undergoing experimental malaria infection have shown that malaria upregulates IFNγ, IL-1ß, and toll-like-receptor-mediated proinflammatory signaling and antigen presentation pathways (8, 9), with similar pathways upregulated in a study of Gabonese children with uncomplicated malaria (10). This evidence concerns the gene IFNG and malaria.