Plasmodium falciparum is now generally considered a cofactor in endemic BL (eBL) that can drive EBV-mediated tumorigenesis by either suppressing the T-/NK-cell immune response to allow EBV-infected B cell proliferation [170], or by the P. falciparum exposure-induced increase in the expression of activation-induced cytidine deaminase (AID) [171], the downstream consequence of which may lead to the hallmark chromosomal translocation of c-myc seen in eBL. This evidence concerns the gene AICDA and Burkitt lymphoma.