Observed differences in expression of proteins directly involved in the secretory process of FGF23, furin and GalNT3, suggest that EPO is not simply an intermediary between iron deficiency and FGF23: furin plays an important role in the upregulation of iFGF23 cleavage in iron deficiency, whereas EPO might act via GalNT3 inhibition as discussed in Section “Erythropoietin” (Hanudel et al., 2018). The gene discussed is EPO; the disease is nutritional disorder.