The effects of TRAP1 on mitochondrial respiration are still controversial: TRAP1 silencing increases oxygen consumption in SAOS-2 osteosarcoma cells, PEA1 ovarian cancer cells, HCT116 colorectal carcinoma cells and mouse fibroblasts [7, 8, 17, 18]; however, TRAP1 silencing or treatment with the mitochondria-directed HSP90 inhibitor Gamitrinibs reduces oxygen consumption and ATP production in PC3 prostate cancer cells and in LN229 glioblastoma cells, although in the specific metabolic context of low glucose availability [9]. The gene discussed is TRAP1; the disease is prostate cancer.