Candida is the most common human fungal pathogen and the cause of invasive candidiasis, the fourth leading cause of nosocomial bloodstream infection in the United States with an estimated annual cost of, US $2 billion and mortality that exceeds 40% despite administration of antifungal therapy in modern intensive care unit facilities [1]. Hence, invasive candidiasis is an unmet medical condition for which better understanding of its pathogenesis at the host–pathogen interface is essential to improve patient outcomes. To that end, a mouse model of the infection, which introduces Candida yeast cells intravenously and mimics skin-derived bloodstream human candidiasis, has been successfully employed to study fungal and host factors that regulate susceptibility to the infection [2].