Eukaryotic organisms require iron to sustain genome stability, cell proliferation and development. Chromosomes contain telomeres to ensure complete replications and avoid fusions. Numerous evidences reveal that iron can act directly or indirectly on telomere maintenance. In human, disruption of systemic or cellular iron homeostasis is reportedly to cause serious health problems such as iron overload (hereditary hemochromatosis), iron deficiency anemia, carcinogenesis and acceleration of aging process. These processes commonly associate with abnormal telomere length. Additionally, cells containing mutations in iron-containing proteins such as DNA polymerases (Polα, δ, and ?), regulator of telomere length 1 (RTEL1) and the small subunit of ribonucleotide reductases (RNRs) have abnormal telomere length. This review briefly summarizes current understandings on iron homeostasis and telomere maintenance in cancer and aging process, followed by discussing their direct and indirect correlation, and the possible regulatory mechanisms.