The investigators who had recorded these facts thought of them only as curious. It is plain, in the first place, however, that this remarkable and rapid multiplication is a proof that senile atrophy is not due to failure of cell proliferation, although the latter has frequently been suggested as the mechanism of senescence. In muscular atrophy, cell multiplication, so far from failing, greatly increases. We may add muscular atrophy to the blanching of hair and the decay of nerve-cells as another instance showing that senile degeneration is not the result of cells ceasing to be able to multiply. Just as in the atrophy of the brain there is an increase in the volume of neuroglœa, the substance in which the neuronophags are found, so also in the atrophy of the muscles there is an increase of muscular nuclei. Along with the increase of nuclei, however, there is an increase of the protoplasmic substance of the fibres known as sarcoplasm. The latter replaces the myoplasm, the specific striated substance of muscles, by a process which must be regarded as parallel with phagocytosis. In a normal muscle the two substances and the sarcoplasmic nuclei are in equilibrium, but in old age the sarcoplasm and its nuclei increase at the expense of the myoplasm. The equilibrium is destroyed with the result that the muscular power is weakened. In these conditions the sarcoplasm acts phagocytically with regard to the myoplasm, just as the chromophag becomes the phagocyte of the pigment of the hair, or the neuronophag devours the nerve-cell. The investigation of other cases of muscular atrophy, as, for instance, that of the caudal muscles of frog-tadpoles, confirms the significance of the process that I have observed in old age. In the two cases, what takes place is the destruction of the contractile material of the muscles by myophags, a special kind of phagocyte.