The majority of cervical cancers have (1) HPVs that hijack ribonucleotide reductase to mint deoxyribonucleotides for replication of viral DNA, or (2) mutations in p53 that abrogate cell cycle restriction checkpoints, free-up ribonucleotide reductase to increase deoxyribonucleotide payout, and replicate DNA unchecked (9). The gene discussed is TP53; the disease is cervical cancer.