Shahangian et al. reported that a decrease in the chemokines CXCL1 and CXCL2 during coinfection with Sp3 rendered the mice more sensitive and that this was linked to type I IFNs by showing that IFN-α/β receptor knockout mice had higher numbers of neutrophils recruited to the lung in response to 2° Sp3 infection (43). The gene discussed is CXCL2; the disease is infection.