We conclude that excess levels of mitochondrial-derived radicals are instantly decomposed by GSH, resulting in normal ROS levels, which prevent any further malignant transformations in oncocytomas, but promote survival and growth (Figure 7), along with the lack of HIF1a stabilization and a stall of glycolytic pathways, which would contribute to increased mitochondrial mass (via PPARGC1B) and prevent malignancy. This evidence concerns the gene PPARGC1B and oncocytic adenoma.