For instance, hypoxia has been shown to drive HMGB1 release from liver cell nuclei,[14] whereas ischemia‐reperfusion promotes its release from brain tissue in ovine fetuses.[15] In addition, hypoxia has been shown to induce the death of certain tumor cells and trigger the release of HMGB1 from the nucleus into the extracellular space, where it acts as a signal to promote tumor angiogenesis.[16] However, the potential molecular mechanisms underlying hypoxia‐induced HMGB1 nuclear export have not been elucidated. The gene discussed is HMGB1; the disease is neoplasm.