The dysfunction of NOS is also related to the reduction of NO bioavailability in malaria, as in Ong et al. [100], who assessed the cerebrovascular capacity and the function of NOS isoforms in cerebral malaria in animals; the loss of eNOS and NOS-I isoforms functionality contributes to cerebrovascular injury, which is characterized by vascular constriction, impaired perfusion, and reduced cerebral blood flow, requiring the recovery of enzymes to increase NO bioavailability. Here, NOS1 is linked to malaria.