One billion people worldwide are affected by fungal pathogens, of which 1.6 million are killed per year more deaths than by malaria and roughly equal to the number of deaths by tuberculosis. A further understanding on how these species adapt to the host and how this influences their pathogenicity is crucial to develop successful strategies to prevent, diagnose and treat fungal infections. Toward this aim, this study introduces the concepts of antivirulence and avirulence genes in human fungal pathogens, based on the well-established concepts of antivirulence genes in bacterial pathogens and avirulence genes in phytopathogenic fungi. Several relevant analogies are presented here, which will help us to understand better the pathogenicity of fungi that infect humans. Candida glabrata is the second most frequent cause of candidiasis despite its inability to cause epithelial damage and inflammatory response in vitro or in mice models. This work shows that C. glabrata seems to rely at least partially on a phenotypic variant, the petite phenotype, which through loss of mitochondrial function can increase its success as a pathogen. Petite phenotype resists high concentrations of azole antifungals and survive better within macrophages. Importantly, a cross-resistance effect between these two exists, showing for the first time a close connection between antifungal resistance and immunoresponse in a pathogenic fungus of humans. In addition, this study elucidates further relevant pathways for the survival and persistence of C. glabrata within macrophages, especially for long-tern events after phagocytosis. These are the metabolism of trehalose and acetate within the phagosome.