Since the cytokine milieu produced in response to infections by pathogenic organisms is known to profoundly influence the quality and effectiveness of adaptive immune responses, it is not surprising that, in response to the coexistence of malaria parasites with humans during the course of evolution and because of the selective pressure by TLR9-activating pathogens, pDCs evolved to express TLR9 and high levels of CD36 for the effective development of immunity to pathogens, including malaria. The gene discussed is CD36; the disease is malaria.