As we previously mentioned, mice deficient in DNA sensor/signaling molecules (cGAS and STING) and RNA sensor/signaling molecules (MDA5 and MAVS) are resistant to infections of the lethal malaria strain YM through the cross‐regulatory mechanism of the early robust production of IFN‐α/β by two type‐I IFN signaling pathways in pDCs.[16, 18] We therefore sought to determine whether such a key regulatory mechanism could be applied to other lethal malaria strains. The gene discussed is CGAS; the disease is infection.