Intriguingly, a more recent study reported that whereas HbAS reduced PfEMP1 expression, adherence to recombinant ICAM-1 and CD36, and adherence to uninfected RBCs, these phenotypic effects were reversed by coinheritance with α-thalassemia [19], mirroring the clinical epidemiology of HbAS, α-thalassemia, and malaria risk [3]. This evidence concerns the gene CD36 and malaria.