The emergence of resistance to the limited arsenal of antifungal drugs impedes the effective treatment of systemic infections12–14. A poignant example is the evolution of resistance to the only new class of antifungal to be approved in decades, the echinocandins15, 16. Echinocandins block β-1,3-glucan biosynthesis in the fungal cell wall via inhibition of the glucan synthase Fks1, thereby compromising cell wall integrity. The most common mechanism of echinocandin resistance involves mutations in the drug target FKS1 17, 18; however, resistance phenotypes are also modulated by cellular stress responses8, 9, 11. Targeting core hubs in cellular circuitry that control responses to stress, such as the molecular chaperone Hsp90 or protein phosphatase calcineurin, has emerged as a powerful strategy to enhance antifungal activity against diverse fungal pathogens8, 16. A challenge in targeting Hsp90 or calcineurin in antifungal drug development is that they are conserved and important regulators in the human host.