IL-12 and IL-18 together, augment IFN-γ production by activating Th1 cells [31], and in our study, despite IL-18 being higher in dengue patients, still had interferon levels that were negligible, implying that IFN-γ production by IL-12 is a co-induction with IL-18 and IL-18 induces IFN-γ only when its receptor is upregulated by IL-12 [30]. This evidence concerns the gene IFNG and dengue disease.