In particular, the upregulation of TFR1, SEC15L1 and MFRN2 mRNAs and down-regulation of FPN1 mRNA suggest an activated response to cytosolic iron deficiency and correlate with increased mitochondrial import; however, the mRNA levels of various enzymes involved in biosynthetic pathways utilizing mitochondrial iron (heme and iron-sulfur cluster) were down-regulated [85]. The gene discussed is TFRC; the disease is nutritional disorder.