CD36 and malaria: Although PS externalization has not been evaluated in P. vivax infection, it was already detected by flow cytometry in RBC infected by P. falciparum, P. berghei, and P. yoelii (41, 58, 59) and in P. falciparum, the binding of late-stage pRBC exposing PS to CD36-expressing cells as well as immobilized CD36 and TSP was inhibited by annexin V, PS-containing liposomes or glycerophosphorylserine—a soluble form of PS (60), indicating that PS could, at least in part, support cytoadhesive phenomena of pRBC in malaria.