NSL1 and malaria: 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.