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Candida albicans is one of the most commonly identified nosocomially acquired pathogens. This organism has a number of virulence traits including production of degrading enzymes, the ability to undergo phenotypic switching, and can rapidly undergo morphogenic switch from a blastospore (yeast) phase to that of a hyphal state. Interest in C. albicans morphogenic regulation has been the focus of a large number of studies, which have characterised transcriptional modulators of these morphologies. Recently, C. albicans has been shown to regulate its morphogenic shift through changes in cell density. It was observed that C. albicans inoculated at cell densities below 106 cells ml−1 under conditions which favour hyphal morphogenesis (pH 7.5, 37 °C), will germinate to form hyphae. However, if cells densities are greater than 106 cells ml−1, little germination will occur and cells will maintain yeast morphology. The basis for this cell-density-dependent control of morphogenesis is similar to that which is seen with bacterial cells regulating their activities via quorum sensing (QS). A number of molecules have been identified which affect the ability of C. albicans to undergo the yeast-to-hyphal shift, and three compounds have been demonstrated to be quorum-sensing molecules. The scope of this review is to bring to light what is now understood about QS in C. albicans and address the roles of these molecules in relation to virulence in the host and potential roles in cross-kingdom interactions.