The rs867186-G is associated with higher levels of sEPCR [17-24], and the addition of recombinant sEPCR inhibits the binding between DC8-expressing parasites and human brain microvascular endothelial cells [7]; therefore, the other possible explanation is that higher levels of sEPCR in malaria patients with the rs867186-GG genotype cause greater inhibition of the binding of DC8 and DC13 PfEMP1 to EPCR on endothelial cells through preferential binding of DC8 and DC13 PfEMP1 to sEPCR compared with EPCR. This evidence concerns the gene CMC2 and malaria.