Recent reports have also demonstrated that when patients infected with Plasmodium falciparum and have secondary infection with EBV receive chloroquine, an agonist of the Ataxia Telangiectasia Mutated kinase and a drug that the parasite is susceptible to, EBV escapes latency and begins to replicate, which coincides with KAP1 pS824 and DNA repair-independent activation of EBV (Li et al., 2017b). This evidence concerns the gene TRIM28 and infection.