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Cancer is most often classified as a genetic disease, with cells accumulating mutations over time that allow for uncontrollable proliferation. However, mutations alone cannot account for all of the phenotypes that cancers exhibit. For example, metastatic cells have distinct morphologies, characteristics, and migratory abilities compared to their primary tumor counterparts, despite having nearly identical genotypes. To understand why this might happen, we must look beyond the genotype of cancer cells and instead focus on their epigenetic landscape, which involves how the genome is folded within the cell and which parts are readily accessible for transcription. This work first investigates how a mutation in the gene liver kinase B1 (LKB1) in lung cancer has the potential to enable metastasis, even though most cells with an identical mutation will never metastasize. Instead, it appears that a specific epigenetic switch must …