Candida spp. rank among the leading causative agents of nosocomial infections. The increasing number of patients at risk of invasive candidiasis makes a rise in the incidence of this fungal infection expected. Disruption of GI tract integrity and ablation of immune cell populations, such as those resulting from cancer chemotherapy, are recognized as key factors leading to fungal dissemination. However, the individual role of these immune barriers in preventing Candida host colonization and invasion are yet to be fully understood. This article evaluates recently published results on a new murine model of systemic candidiasis originating in the GI tract that might prove a valuable setting for the accurate study of host immune mechanisms, fungal virulence factors and novel therapeutic approaches.