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Underlying the resilience of this parasite is its remarkable ability to undergo genome modifications, thus, providing parasite populations with extensive genetic variability that accelerates selection of drug resistance and limits the efficacy of most vaccines. This genome plasticity is rooted in the mechanisms of DNA repair that parasites employ to maintain genome integrity, a process skewed toward homologous recombination through the evolutionary loss of classical nonhomologous end joining. Repair of DNA double\u2010strand breaks have been shown to enable \u201cshuffling\u201d of antigen\u2010encoding gene sequences to vastly increase antigen diversity and to enable copy number expansion of genes that contribute to drug resistance. The latter phenomenon has been proposed to be a major contributor to the rise of resistance to several classes of antimalarial drugs. In this issue of <jats:italic>Molecular Microbiology<\/jats:italic>, McDaniels and colleagues add yet another mechanism that malaria parasites use to reduce drug susceptibility by demonstrating that <jats:italic>P. falciparum<\/jats:italic> can maintain expanded arrays of drug resistance cassettes as stably replicating, circular, extrachromosomal DNAs, thus, expanding genome plasticity beyond the parasite\u2019s 14 nuclear chromosomes.<\/jats:p>","DOI":"10.1111\/mmi.14632","type":"journal-article","created":{"date-parts":[[2020,10,26]],"date-time":"2020-10-26T11:34:15Z","timestamp":1603712055000},"page":"503-507","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":10,"title":["The contribution of extrachromosomal DNA to genome plasticity in malaria 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