FECH encodes ferrochelatase, a mitochondrial enzyme that catalyzes the terminal step of heme biosynthesis by inserting ferrous iron into protoporphyrin IX 12. This enzyme is essential for heme production and red blood cell development, as evidenced by its upregulation during high-altitude acclimatization where enhanced oxygen-carrying capacity is needed 3. FECH deficiency causes erythropoietic protoporphyria (EPP), an autosomal dominant disorder characterized by painful photosensitivity due to protoporphyrin IX accumulation in erythrocytes and tissues 12. EPP patients typically present with cutaneous symptoms upon sun exposure and may develop hepatic complications, as protoporphyrin is excreted through the liver 1. The disease often involves inheritance of loss-of-function FECH mutations combined with a hypomorphic allele 12. Interestingly, EPP patients frequently exhibit microcytosis even without iron deficiency, suggesting heme deficiency despite normal iron availability 4. Beyond EPP, FECH has broader clinical relevance, with genetic variants associated with migraine susceptibility 5 and antituberculosis drug-induced liver injury 6. The gene's regulation involves epigenetic mechanisms, as SETD2-mediated H3K36me3 modification controls FECH transcription and affects cellular sensitivity to ferroptosis 7.