Moreover, since telomere dysfunctions trigger a profound inhibition of mitochondrial biogenesis through p53-mediated suppression of both PGC-1α and PGC-1β [124], loss of function of this tumor suppressor adds a layer of complexity to the amount of stress that a cancer cell can adapt to before triggering mitochondria-mediated apoptosis. This evidence concerns the gene PPARGC1A and neoplasm.