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 threshold of detection but subsequently expanded due to positive selection. Further work is required to begin to unravel the underlying mechanisms that result in mosaic abnormalities, particularly as it relates to how and when altered clones are created, tissue-specificity, and the timing and expansion of distinct populations of cells with age. Finally, these findings underscore the importance of considering the role and time-dependent nature of somatic events in the etiology of cancer as well as other late-onset diseases.
