During hypoxia or iron deficiency, PHDs are inactivated, HIF-1α hydroxylation is inhibited, HIF-1α subunits become stable and dimerize with HIF-1β, forming an HIF complex via ARnt-mediated transfer from cytoplasmic to nuclear, possibly interacting with HIF-αβ transcription complex to further activate hypoxia. The gene discussed is HIF1A; the disease is nutritional disorder.