摘要:SummaryHuman fungal pathogens are the causative agents of devastating diseases across the globe, and the increasing prevalence of drug resistance threatens to undermine the already limited treatment options. One prominent pathogen is the opportunistic fungusCandida albicans, which can cause both superficial and serious systemic infections in immunocompromised individuals.C. albicansantifungal drug resistance and antifungal tolerance are supported by diverse and expansive cellular stress response pathways. Some of the major players are the Ca2+-calmodulin-activated phosphatase calcineurin, the protein kinase C cell wall integrity pathway, and the molecular chaperone heat shock protein 90. Beyond these core signal transducers, several other enzymes and transcription factors have been implicated in both tolerance and resistance. Here, we highlight some of the major stress response pathways, key advances in identifying chemical matter to inhibit these pathways, and implications forC. albicanspersistence in the host.Graphical abstractDisplay OmittedHighlights•Candida albicanscan cause superficial and serious systemic infections in humans•Stress response pathways regulateC. albicansantifungal resistance and tolerance•Stress response regulators include calcineurin, Pkc1, Hsp90, and many others•Stress response inhibitors could reduce the likelihood of fungi persisting in humans