Since most cancer cells show evidence of a period of early genomic instability that appears to stem from telomere dysfunction [47], a short lapse in the normal elimination of such cells may be sufficient to allow genomic reshuffling that can facilitate carcinogenesis, partially accounting for the increased incidence of cancer in humans that are heterozygous for p53 and Chek2 mutant alleles. The gene discussed is TP53; the disease is cancer.