Infectious diseases caused by fungi are considered emerging diseases. Recently, the World Health Organization (WHO) has published a report recognizing the threat that these eukaryotic pathogens pose to public health. These infections are part of a silent pandemic due to the increase in their incidence, especially among immunocompromised populations. The rise in antifungal resistance and the limited arsenal available against eukaryotic pathogens make fungal infections particularly difficult to treat and associated with high rates of morbidity and mortality. Antifungal resistance generated through epigenetic mechanisms is transient and unstable: it appears under selective pressure, for example, the temporary administration of antifungal treatment, and disappears when the selective pressure ceases. To combat this problem, it is crucial to understand the full spectrum of epigenetic mechanisms and their in vivo interactions that contribute to adaptations in fungal pathogens. We use Mucor circinelloides, a pathogenic fungus that causes a severe infection called mucormycosis, as an example to characterize antifungal resistance mechanisms.