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demonstrated that the knockdown of SLC25A39 in murine erythroleukemia cells impaired iron incorporation into protoporphyrin IX, while a yeast mutant of the SLC25A39 gene exhibited an iron homeostasis defect, which could be restored by the vertebrate SLC25A39 [30]

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In the European guidelines [8, 9], the management of this group has never been properly described from a practical point of view, i.e