NCOA4 mediates iron mobilization from liver ferritin stores. HIF-1α and HIF-2α are stabilized under conditions that inhibit the activity of the prolyl hydroxylases that regulate HIF (eg, iron or oxygen deficiency, presence of small molecule inhibitors). HIF-driven transcription promotes expression of NCOA4, which is stable under conditions of iron deficiency. NCOA4 directs ferritin to the autolysosome for degradation, and iron released from ferritin is transferred to the cytosol for export via ferroportin. See Figure 7D in the article by Li et al that begins on page 2691.