Cells employ many strategies to avoid genetic mutation. From the high fidelity of DNA-synthesizing enzymes to the pro-death signaling that accompanies mutagenic stimuli such as UV radiation, cellular mechanisms that stymie genetic changes are ubiquitous throughout the natural world. These mechanisms are critical because widespread genomic changes would 5 wreak physiological havoc; indeed, malfunctions in molecular players that safeguard against mutagenesis, such as the protein p53, have been implicated in diseases such as cancer. Yet despite the criticality of preventing and eliminating DNA mutations to avoid deleterious changes in cells, in specific contexts many organisms have also adapted beneficial mechanisms to induce genetic changes. One such instance is observed in vertebrate immune systems: white blood cells such as T cells recognize invading pathogens through receptors on their surfaces. In order to recognize a wide variety of pathogens, these cells must generate a large repertoire of receptors. Relying only on a genetically encoded repertoire would be disadvantageously limiting – analogous to having only a few dozen language phrases with which to respond to the nearly infinite potential combinations of words in a conversation. Instead, the repertoire is generated by a process of genetic recombination, in which T cells "cut-and-paste" the DNA encoding their microbe-recognizing receptors. Many of these genetic rearrangements produce cells bearing non-functional proteins; such unproductive cells are eliminated through senescence. Nevertheless, this seemingly haphazard process of programmed genetic mutation is crucial to generating immunological diversity, as individuals with defects in this pathway exhibit clinical immunodeficiency. How this process is regulated by T cells to prevent harmful mutations remains the subject of ongoing research.