Furthermore, in this same investigation, NETosis mediated vasculature inflammation by immunostimulating the emergency granulopoiesis in macrophages via granulocyte colony-stimulating factor (G-CSF) and by upregulating ICAM-1, an important receptor of cytoadhesion, which mediates the sequestration of iRBC in brain and liver microvasculature, therefore being a key mediator of cerebral malaria as well as liver and lung injuries (Figure 5B). Here, CSF3 is linked to cerebral malaria.