Over 80% of the world’s population suffer from serious fungal infections with systemic candidiasis reaching a high mortality rate of 30-40% (1). Multiple Candida species can be pathogenic to humans, and of them Candida albicans is the most frequent. C. albicans is a commensal microbe, but patient immunosuppression, prolonged antibiotic therapy or use of devices can trigger pathology. Pathology is associated with a morphological transition from yeast to hyphal forms (2). Also, the past decade has seen an increase in occurrence of antifungal-resistant strains which has prompted research to focus on new molecular mechanisms that may increase the susceptibility of C. albicans towards antifungal drugs. We have recently identified that the small molecule inhibitor Mdivi-1 represses hyphal growth of C. albicans (3). Although the molecular target of Mdivi-1 has been proposed to be the mitochondrial division GTPase Dnm1 (Drp1 of mammals), Mdivi-1’s effects on hyphal morphogenesis in C. albicans were not recapitulated by homozygous deletion of DNM1. Our RNAseq data showed that Mdivi-1 triggered large transcriptional reprogramming in hyphae, which was consistent with cells experiencing metabolic stress. Mdivi-1 also led to a reduction of nitric oxide levels, and by investigating this mechanism further we defined for the first time a role for endogenous nitric oxide signalling is hyphal morphogenesis of C. albicans. Multiple genes encoding transcription factors and other signalling proteins were differentially expressed in Mdivi-1-treated cells. We are currently addressing their roles in hyphal morphogenesis, and also extending the study to other stressors and antifungal therapeutics.