In glioblastoma, inhibition of HSP60 leads to the increased formation of reactive species (ROS) in mitochondria, subsequently exerting the complex I inhibitor retenone-induced AMPK activation, which in turn suppresses mTORC1-mediated phosphorylation of S6K and 4EBP1 and deactivates the protein translation machinery and cancer cell growth [33]. Here, HSPD1 is linked to cancer.