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His research revealed the first link between a human tumor suppressor gene, p53, and the control of genetic stability, establishing the principle that disabling genes that guard the genome accelerate cancer. He then elucidated a variety of mechanisms by which  p53 functions, including preventing proliferation of cells that have trace amounts of DNA damage or that are experiencing metabolic stresses without DNA damage. This foreshadowed metabolic imbalance sensing as an important theme in cancer biology. His lab developed mouse models revealing the tissue specificity and sensitivity of the p53 stress sensor in vivo, and how this can impact radiation sensitivity and cancer predisposition. Recent work in his lab interrogating relationships between stem cells and cancer set the precedent that cells within aggressive breast cancers resemble breast stem cells that arise during embryogenesis, suggesting that adult cells may reprogram to this state to generate cancer. HIs lab has developed important molecular and genetic manipulation technologies with broad impact in biology, exemplified by methods to accelerate nucleic acid hybridization and site-specific recombinase systems for use in metazoan genomes.