Replicative senecence, is not a cell death but characterised by an irreversible cell cycle arrest, resistance to apoptosis and varibilites in gene expression and functions. There are both telomeric and non-telomeric pathways regarding senecence. The major etiology depends on Lelomeric instability. Apoptosis is a genetically programmed cell death and p53 is very important in the regulation of senescence. The senescent CD8 T-cells have effects on both immune on non-immune systems. The deterioration of T-cell functions with ageing is called as immunosenecence. Telomere shortening is the main cause of human progeroid syndomes. Increase in premature cellular senescence and /or apoptosis have been found in Werner syndrome, Hutchinson-Gilford progeria syndrome and Cockayne syndrome. Ageing is related with telomere shortening. Ageing can be accepted as a multifactorial and variable entity. Telomere length can be used as a biological marker in the etiology of biological ageing. As a conclusion, arrays can be designed to evaluate lots of genes in order to clarify the mechanisms of senescence.