Febrile malaria episodes that are more likely among women with low immunity are thought to induce uterine contractions, which are mediated by elevated levels of tumour necrosis factor-α (TNF α) leading to preterm birth [34, 49]; whilst Gallego-Delgado and Rodriquez provided supporting information that angiotensin II (Ang II) may protect against cerebral malaria, possibly via its effects on host vascular endothelial cells [50]. Here, AGT is linked to cerebral malaria.