While myeloid-specific deficiency of clock components exacerbated inflammatory responses and sepsis upon CLP or L. monocytogenes infection [17, 27], myeloid-specific Bmal-deficient mice controlled bacterial replication better and suffered less weight loss during S. aureus infection, which was attributed to enhanced macrophage motility and phagocytosis [21]. The gene discussed is CLOCK; the disease is Sepsis.