Candida albicans, the most prevalent human fungal pathogen, is generally diploid but other ploidy states clearly arise and are found not only in the laboratory but also in clinical isolates.  A major question motivating our work is how ploidy state and ploidy shifts affect pathogen evolution and survival, especially in responses to extreme stresses, such as exposure to antifungal drugs within the host. Survival of these stress conditions can be due to drug resistance, tolerance or persistence and we are interested in the degree to which each of these strategies is used as well as the molecular mechanisms used to achieve these different strategies.  We are also particularly interested in how rapidly these different strategies can be recruited to assist in stress survival.  An important clue comes from the observation that 50% of isolates that are resistant to fluconazole (FLC), the most widely used antifungal, are aneuploid and that some specific aneuploidies can confer FLC resistance.  Is aneuploidy the cause of resistance or does exposure to antifungals promote the appearance of aneuploidy? Our work indicates that the answer is yes: aneuploidy can be both a cause of drug resistance and a consequence of drug exposure.  Furthermore, drug exposure elicits changes in cell cycle progression that lead to whole ploidy shifts. We have been following the fate of tetraploid cells as well as the evolution of diploids in the presence of drug to determine the relationship between ploidy state and shifts in ploidy state provide rapid responses to drug and how such responses affect the evolution of survival in drug stress.