Interestingly, expression of the LTβR is essential for the development of experimental cerebral malaria (ECM) after infection with Plasmodium berghei ANKA and prolongs survival in LTβR−/−-deficient mice due to their inability to generate an effective (CD8+) T cell response, which is responsible for ECM pathophysiology [53, 54]. The gene discussed is CD8A; the disease is infection.