FTH1 and triple-A syndrome: FTH1 may also physically interact with several signaling elements involved in critical cellular pathways, such as the C-X-C Motif Chemochine Receptor 4 (CXCR4) receptor, expressed in a variety of human malignancies and ALADIN protein (alacrima-acalasia-adrenal insufficiency neurological disorder), whose mutations determine the triple-A syndrome characterized by a deficiency of FTH1 nuclear import [44,45]; moreover, FTH1 binds, stabilizes, and activates p53 under oxidative stress [46].