HSPD1 and cerebral cavernous malformation: Remarkably, in cellular models of CCM disease, these modifcations affect proteins involved in cellular homeostasis and adaptive responses to stressful conditions, including prominent members of the heat-shock protein (HSP) family functioning as molecular chaperones, such as HSP70, HSP27, and HSP60; enzymes of energy metabolism; and cytoskeleton proteins, suggesting that they play an important role in the chronic adaptive redox homeostasis and enhanced cell susceptibility to OS and inflammation that have been associated with loss-of-function mutations of CCM genes [48].