In vitro experiments showed that Plasmodium‐parasitized erythrocytes could induce human peripheral monocytes to release HMGB1, demonstrating that the increase in HMGB1 in patients with persistent P. falciparum infection may prolong the inflammation and fever of malaria, but unfortunately, treatment with the HMGB1 neutralizing antibody in an experimental mouse model of severe malaria did not reduce mortality.39 Here, HMGB1 is linked to malaria.