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Human telomere length encompasses a normal range with discrete upper and lower limits. Both longer and shorter telomeres have been linked to cancer. In the first case, the association lies in the presence of mutations promoting telomere elongation. Longer telomeres may favor a delayed cell senescence, increasing the opportunities to develop genomic instability, thus the risk of carcinogenic transformation. On the other hand, shorter telomeres can be a direct source of genomic instability. Unstable, dysfunctional telomeres are recognized as DNA damage sites and can promote chromosomal rearrangements ultimately leading to genome alterations that favor cancer development. In both cases, telomere length plays a pivotal role in the survival of cancer cells.