(a) Telomere length can be prevented from shortening by an enzyme Telomerase. Telomerase has a protein subunit (hTERT) and an RNA subunit (hTR). This enzyme is active in germline and stem cells and maintains their telomere length by adding ‘TTAGGG’ repeats to the ends of chromosomes. Therefore, telomeres do not shorten in these types of cells. (b) Telomerase is inactive in normal somatic cells. These cells, therefore, lose telomeres over time and when telomere length reaches below a critical limit, cells either senesce or die. (c) In the absence of appropriate signals for senescence or apoptotic death, continued cell division leads to severe telomere shortening and genomic instability. Although rare, but cells which survive this crisis, activate a telomere maintenance mechanism (either telomerase or homologous recombination-based ALT) and may become oncogenic. Therefore, most cancer cells have very short but stable telomeres. TA, telomere attrition; TL, telomere length.