This review discusses the molecular and cytokinetic aspects of cellular aging of human diploid fibroblasts. Despite a large amount of data, the basis of their limited life span has not been defined. A replicative defect in aging cells lies in the mechanism(s) that initiates DNA synthesis, and the control of this mechanism(s) is mediated through an alteration in the synthesis of specific RNA and protein molecules. Two major groups of hypotheses have been offered to explain these findings. The differentiation hypotheses are based on the concept of a ‘biological clock’, while error hypotheses presuppose defects in genetic transcription or translation.