We have extended our initial observation that detectable clonal mosaicism of the autosomes is present in the population with surprising frequency and particularly in the aging genome. A recent study of detectable clonal mosaicism in twins reported an increase in frequency with age and suggested that this reduction could lead to a less diverse blood cell population and immune system15. These emerging data raise a number of critical issues in mechanisms underlying the possible shift in the repertoire of clones with large structural abnormalities. Thus cells with abnormal karyotypes could have an early developmental origin in which a somatic event in a single stem cell progenitor during embryogenesis could become apparent when cellular diversity decreases with age and cell populations become increasingly oligoclonal. Higher rates of detectable clonal mosaicism in older cancer-free individuals could also be due to increased rates of somatic mutation or diminished capacity for genomic maintenance, such as with telomere attrition34 leading to proliferation of somatically altered cell populations. A survival bottleneck of cellular progenitors could also lead to observable mosaic alterations that were previously below the
