The mouse model of experimental cerebral malaria (ECM) induced by infection with Plasmodium berghei ANKA (PbA) has been used extensively to demonstrate the critical role of myeloid cells (neutrophils, dendritic cells, macrophages), CD4+ and CD8+ T cells and NK cells in the pathogenesis of acute neuroinflammation, and to establish the role of pro-inflammatory mediators (e.g., TNF, type I and type II IFN, IL1b, MIP1a, MIP1b/CCL4, CXCL1, CXCL9, CXCL10)4. This evidence concerns the gene CCL4 and cerebral malaria.