In the murine model of malaria, proinflammatory cytokines, such as IFN-γ and IL-12, are required to control the parasite load in the circulation [4]. P. falciparum experimental infection of individuals who never had malaria caused an increase in the levels of circulating proinflammatory biomarkers IFN-γ, IL-12p40, and CXCL-8 at the time of the appearance of parasitized erythrocytes [5]. The gene discussed is CXCL8; the disease is malaria.