With evidences of massive inflammatory cytokines (TNF-α, IL-1, IL-4, IL-6, and IL-12) associated with HIF-1α expression, HIF-1α was proven as a critical determinator for sepsis phenotype.129 Similar signs of altered metabolism were later observed in activated innate immune cells (dendrite cells and macrophages).130,131 During sepsis, presence of hypoxia, inflammatory, or infectious signals prevented HIF-1α from degradation. The gene discussed is IL1B; the disease is Sepsis.