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<i>Candida auris</i> has simultaneously emerged on five continents as a fungal pathogen causing nosocomial outbreaks. The challenges in the treatment of <i>C. auris</i> infections are the variable antifungal susceptibility profiles among clinical isolates and the development of resistance to single or multiple classes of available antifungal drugs. Here, the <i>in vitro</i> susceptibility to echinocandin antifungal drugs was determined and <i>FKS1</i> sequencing was performed on 106 <i>C. auris</i> clinical isolates. Four isolates were identified to be resistant to all tested echinocandins (MIC ≥ 4 mg/liter) and harbored an S639F mutation in <i>FKS1</i> hot spot region 1. All remaining isolates were <i>FKS1</i> wild type (WT) and echinocandin susceptible, with micafungin being the most potent echinocandin (MIC<sub>50</sub> = 0.125 mg/liter). Antifungal susceptibility testing with caspofungin was challenging due to the fact that all <i>FKS1</i> WT isolates exhibited an Eagle effect (also known as the paradoxical growth effect), which occurred at various intensities. To assess whether the Eagle effect resulted in pharmacodynamic resistance, 8 representative isolates were evaluated for their <i>in vivo</i> drug response in a murine model of invasive candidiasis. All isolates were susceptible to caspofungin at a human therapeutic dose, except for those harboring the S639F mutation. The data suggest that only isolates carrying mutations in <i>FKS1</i> are echinocandin resistant and that routine <i>in vitro</i> testing of <i>C. auris</i> isolates for susceptibility to caspofungin by the broth microdilution method should be viewed cautiously or avoided.