To avoid degradation and the mechanisms of DNA double strain break repair, linear eukaryotic chromosomes have developed telomeres – the specific DNA-protein structures comprised of repetitive TTAGGG nucleotide sequences. Due to the nature of DNA replication every division makes telomeres shorter. Because of this, the number of divisions is set by telomere length. Short telomeres are factors of genetic instability. The most significant cause of genetic instability lies in the fusion-bridge-fusion cycle (B/F/B) which leads to nonreciprocal translocations, DNA fragmenting and duplications of the whole chromosome or even genome. Cells can escape death caused by short telomeres by reactivation of telomerase, RNA-dependent DNA polymerase usually active only in embryotic cells, or by the alternative lengthening of telomeres (ALT). In vitro reactivation of telomerase leads to cell immortalization while in vivo active telomerase means tumour development. Telomerase is active in over 90% of all tumours and inactive in normal healthy somatic cells. Because of this, telomerase inhibitors play a crucial role in the development of anti-cancer therapeutics.