Our findings point to a ‘two-phase’ model for disease progression (Fig. 6), which relies on a decision-sensing system that responds to CXCL10 levels: during early infection (or non-CM) malaria, when there is a tightly regulated immune response, the parasite modifies the immune response by inhibiting CXCL10 translation in monocytes (Fig. 6, upper panel), as supported by low CXCL10 levels in clinical samples of non-CM malaria patients11. This evidence concerns the gene CXCL10 and infection.