Such oxidatively stressed RBCs then serve to facilitate macrophage activation by binding macrophage Fc receptors; indeed, with respect to malaria protection, it has been theorized that protection conferred by G6PD deficiency may be related to increased phagocytosis of parasitized oxidatively-damaged G6PD-deficient RBCs (77–79) via binding by macrophage Fcγ and lectin-like receptors (80), and that such parasites may be more susceptible to ROS (81). Here, G6PD is linked to malaria.