The experimental evidence is reviewed which bears on the theory that aging in mammalian cells may be related to a decline in the efficiency of normal DNA repair processes. Although the data are as yet fragmentary, they do suggest that there is an age-associated decline in the capacity of cells to perform at least certain types of repair. This is particularly noticeable in human diploid cells as they reach terminal senescence in vitro. Whether this decline is causally related or even contributory to normal aging remains, however, an open question.