Even more surprising is the finding that at 40 hours of infection, when the bacterial loads in the lungs of LysM-cre × Hif1αfl/fl mice were higher than those of littermate controls, lung cytokine levels were not higher anymore, suggesting a bimodal effect of myeloid HIF1α on cytokine production in the lungs (inhibitory early after infection while—relatively—enhancing later on, during fulminant sepsis). This evidence concerns the gene HIF1A and infection.