Although it is conceivable that the MAVS‐, STING‐, and inflammasome‐mediated signalling pathways converge to induce SOCS1 expression to modulate TLR7‐MyD88‐IRF7‐dependent type I IFN response during malaria infection, there is still lack of systematic analysis of underlying mechanisms in (a) what exact role does the MAVS‐, STING‐ or inflammasome‐mediated pathway play in anti‐malaria immunity, and (b) how these dynamic networks cooperatively response to varying dose or time of YM challenging. Here, MAVS is linked to malaria.