Chromatin regulation has been reported to contribute to fungal pathogenesis, as inactivating mutations of histone acetyltransferases (HATs) or histone deacetylases (HDATs) cause decreased virulence of the human fungal pathogen Candida albicans.In addition to acetylation, these enzymes are able to modify histones with other acyl marks, such as histone crotonylation (HKcr), a recently discovered active mark that, similarly to acetylation, leads to gene transcription. Histone crotonylation is “read” by the YEATS domain, which is highly conserved from humans to yeast and found in subunits of chromatin remodelling complexes and general transcription factors. Although histone crotonylation is presumed to be controlled by metabolic and developmental signals, its cellular roles are poorly understood, and the functions of the YEATS proteins have been studied very little outside of humans and the model yeast Saccharomyces cerevisiae. We performed a comprehensive bioinformatic analysis of YEATS domain proteins in fungi, including human fungal pathogens, which revealed that the YEATS domain is conserved, and pathogens encode 1 or 2 YEATS proteins. Deletion of either YEATS-encoding gene in C. albicans, TAF14 or YAF9, leads to reduced fitness and compromises virulence in the mouse tail vein infection model. The taf14∆∆ mutant displays morphogenesis defects in both yeast and hyphal growth, is sensitive to membrane-damaging drugs (DMSO and formamide), but resistant to cell wall stress induced by calcofluor white or congo red. Some, but not all of these phenotypes were recapitulated by the taf14W80A mutant in the YEATS domain. In conclusion, the YEATS domain chromatin readers play important roles in fitness and virulence of C. albicans via YEATS-dependent and YEAST-independent roles.