This link between EBV and endemic Burkitt lymphoma, while suspected to be in part a consequence of malaria-induced immunosuppression as well as induction of activation-induced cytidine deaminase in B cells [68], may be further compounded by high EBV loads caused by the routine non-prescription use of the antimalarial drug chloroquine, which activates the EBV lytic cycle by activation of ATM and ATM-mediated phosphorylation and inactivation of KAP1, resulting in dysregulation of heterochromatin [14]. This evidence concerns the gene ATM and Burkitt lymphoma.