The term 'cellular senescence' has often been applied indiscriminately to any form of growth arrest of cultured cells that occurs either after some period in culture or following insults such as the overexpression of oncogenes. Recent reports have suggested there may be many mechanisms of cellular senescence. Our increasing understanding of the role of telomere shortening in the replicative aging of cultured fibroblasts now permits a re-examination of what may reasonably be called cellular senescence, and what most likely represents artifacts of the culture environment and/or specific cell-cycle control mechanisms.