The human fungal pathogen is RNAi-deficient and lacks active transposons in its genome. has regional centromeres that contain only transposon relics. To investigate the impact of centromere loss on the genome, either centromere 9 or 10 was deleted. Deletion of either centromere resulted in neocentromere formation and interestingly, the genes covered by these neocentromeres maintained wild-type expression levels. In contrast to ∆ mutants, ∆ mutant strains exhibited growth defects and were aneuploid for chromosome 10. At an elevated growth temperature (37°C), the ∆ chromosome was found to have undergone fusion with another native chromosome in some isolates and this fusion restored wild-type growth. Following chromosomal fusion, the neocentromere was inactivated, and the native centromere of the fused chromosome served as the active centromere. The neocentromere formation and chromosomal fusion events observed in this study in may be similar to events that triggered genomic changes within the / species complex and may contribute to speciation throughout the eukaryotic domain.