Heat shock protein required for pathogenicity. Mediates thermotolerance and adaptation to oxidative stress and ethanol-induced stress. Required for invasive growth and filament formation under various filament inducing conditions. Plays a role in the capacity of damaging human-derived endothelial and oral epithelial cells during infection. Potentiates resistance to antifungal drugs, as well as resistance to killing by human neutrophils. Plays a major role in trehalose homeostasis in response to elevated temperatures. Regulates CEK1 activation by phosphorylation in response to elevated temperatures. Only expressed in stationary phase. Expression is increased in the absence of adenylyl cyclase and in biofilms. Belongs to the small heat shock protein (HSP20) family.