Candida albicans is a diploid yeast that causes opportunistic infections in humans. There is growing evidence indicating that during the infection process, the success of the organism relies to a large extent on its ability to adapt to the several niches in the human host through genetic changes, mainly point mutation, loss of heterozygosity (LOH), and aneuploidies. The genetic plasticity of C. albicans is likely derived, at least in part, from its obligate diploidy and is manifested in the karyotype variability found among the clinical isolates. These genetic changes may also contribute to the maintenance of a commensal and opportunistic life history of C. albicans. Since mutation, LOH, and aneuploidy rates are under the control of the DNA replication/repair/ recombination machinery, the analysis of mutation/recombination processes and mechanisms may help to understand the biology and pathogenesis of this fungus.