Telomeres are non-coding protective sequences found at the end of linear chromosomes. They are made of repeating sequences, for example TTAGGG in vertebrates, and proteins that protect them and participate in their function. One of their functions is to distinguish the ends of the chromosomes from double-strand breaks – to prevent a cellular repair mechanism (NHEJ) from 'repairing' them which would lead to chromosome fusion and rearrangements, and, eventually, cell crisis or cancer. Because of the chromosome end replication problem, DNA is shortening with every cell division. In order to preserve genes from eroding, telomeres are the ones that are being lost, for until they reach the Hayflick limit when the cell stops dividing because of unprotected chromosomes. Some cells and noncellular organisms express an enzyme called telomerase which lengthens telomeres with its RNA template and protein domain. Telomerase is expressed, for example, in stem and cancer cells. The later have succeeded to shut down pRB and p53 pathways that would lead to cellular senescence or apoptosis, and to increase the activity of telomerase, making themselves immortal. Cancer cells also use alternative telomere lengthening mechanisms that include homologous recombination. It is assumed that senescence has evolved in a way to prevent tumorigenesis. Scientists, however, have succeeded to slow down ageing in mice with telomerase, without an increase in tumour occurrence. Telomere shortening is one of the reasons why we age, so future research could find a way to expand human lifespan. Additionally, vaccines for cancer based on telomerase are already being tested, with successful results.