CD36 and cerebral malaria: The SNPs found in Kenya and Gambia introduce a premature stop codon that results in a truncated CD36 protein lacking the C-terminus and is therefore incompetent for signal transduction but can still bind its ligand(s), leading to the conclusion that mutations that cause CD36 deficiency may reduce CD36-mediated parasite sequestration in peripheral organs but they may not protect from severe cerebral malaria (Aitman et al., 2000) that is associated with cyto-adherence to brain endothelium via interactions of PfEMP-1 with ICAM-1 but not CD36 (Ockenhouse et al., 1991).