The human pathogenic fungusCandida glabratais the second leading cause of candidemia, a life-threatening invasive mycosis. Clinical outcomes are complicated by reduced susceptibility ofC. glabratato azoles together with its ability to evolve stable resistance to both azoles and echinocandins following drug exposure. Compared to otherCandidaspp.,C. glabratadisplays robust oxidative stress resistance. In this study, we investigated the impact ofCgERG6gene deletion on the oxidative stress response inC. glabrata. CgERG6gene encodes sterol-24-C-methyltransferase, which is involved in the final steps of ergosterol biosynthesis. Our previous results showed that theCgerg6Δmutant has a lower ergosterol content in its membranes. Here, we show that theCgerg6Δmutant displays increased susceptibility to oxidative stress inducing agents, such as menadione, hydrogen peroxide and diamide, accompanied with increased intracellular ROS production. TheCgerg6Δmutant is not able to tolerate higher concentrations of iron in the growth media. We observed increased expression of transcription factors,CgYap1p,CgMsn4p andCgYap5p, together with increased expression of catalase encoding theCgCTA1gene and vacuolar iron transporterCgCCC1in theCgerg6Δmutant cells. However, it seems that theCgERG6gene deletion does not influence the function of mitochondria.