Indeed, in a murine model of malaria and bacterial coinfection, it was demonstrated that acute Plasmodium infection induces high levels of pro–caspase-1 in monocytes, which resulted in elevated levels of activated caspase-1 and extraordinarily high levels of the proinflammatory cytokine IL-1β after bacterial infection, culminating in a dramatic increase in mortality (9). This evidence concerns the gene CASP1 and malaria.