In contrast, the administration of IL-18 accelerated atherosclerosis in apolipoprotein E-deficient mice via an interferon-γ (IFNγ)-dependent mechanism [52], suggesting that likely targets of IL-18 during atherogenesis are immune cells, such as CD4+ T cells [14,53], eliciting IFNγ production and the subsequent upregulation of pro-inflammatory responses [54]. The gene discussed is IFNG; the disease is atherosclerosis.