ATR and Seckel syndrome: The rapid exhaustion of replication ability in ATR-deficient cells may explain the rarity of tumors either in ATR null mice or in human Seckel syndrome [63] or even the small occurrence of tumors in heterozygous mice suggesting that unrepaired DNA is incompatible with cell life, reinforcing the view that sustained cell proliferation must be supported by a putative anomalous telomere-associated mechanism rather than by genomic mutation; in other words, unrepaired DNA leads to cell death rather than cancer.