G6PD and malaria: Thus, the coupled host-pathogen model allowed us to connect previous observations on 1) the inhibition of the host glycolysis by the malaria parasite [5], 2) the parasite-exacerbated oxidative stress faced by RBCs [41], 3) the ribulose-5-phosphate secretion induced by P. falciparum infection [16], and 4) the malarial resistance for G6PD-deficient patients [42] into a single coherent metabolic description of the oxidative stress response.