Starting with this result, the authors then asked whether TRAP1 is important for the mitochondrial respiration of prostate cancer cells and found that exposure to the small molecule Gamitrinib, which inhibits both mitochondrial HSP90 and TRAP1, led to decreased OCR and that TRAP1 silencing halted the increase of compensatory OCR induced by glucose deprivation. This evidence concerns the gene TRAP1 and Familial prostate cancer.