Candida auris recently emerged as a serious fungal pathogen that can cause invasive candidasis with mortality rates as high as 60%; however, little is known about the pathogenesis of C. auris and it is unclear why it is spreading rapidly in hospitals. In a recent study, Johnson et al. investigated the interaction between C. auris and neutrophils, which control invasive candidasis through phagocytosis or by releasing neutrophil extracellular traps (NETs). In a co-culture in vitro system, human neutrophils were poorly recruited and killed C. auris at lower levels compared to Candida albicans. Moreover, these neutrophils failed to form NETs. When neutrophils were mixed with both C. auris and C. albicans, neutrophils preferentially interacted with and killed C. albicans. When these Candida species were injected into zebrafish larvae hindbrains, ~50% fewer neutrophils were recruited to C. auris, and NETs were only produced in the presence of C. albicans, suggesting that the evasion of neutrophils contributes to the virulence of C. auris.