As discussed under section 1.2.1, HsClpP is known to provide stress relief from the accumulation of ROS by mediating the turnover of specific subunits of OXPHOS complexes. In cancer cells, increases in the level of intracellular ROS is important for facilitating and sustaining oncogenesis.Thus, increasing the level of expression of HsClpP may serve as a coping mechanism for these cells to grow and proliferate under increased intracellular ROS with increased risks of protein misfolding and aggregation. In support of this notion,heat shock proteins (HSPs) and molecular chaperones are known to be overexpressed in cancer cells to protect against the deleterious effects of accumulated oncogenic mutationsand death by ROS-induced apoptosis. Importantly, these proteins may serve as potential anticancer drug targets by circumventing the cancer cell’s ability to cope with elevatedROS levels. By the same premise, the potential of HsClpP as an anticancer therapeutic target has been explored, leading to the discovery and development of small molecule compounds that can specifically target and modulate the proteolytic activity of HsClpP.