A defective ATP synthase combined with an increase in mitochondrial biogenesis regulating factors (PGC-1α related co-activators i.e. PRC) has been evaluated in oncocytic models, which is also suggestive of the fact that decreased mitochondrial function is compensated by an increase in mitochondrial biogenesis to support the bioenergetic demands of the proliferating tumor (Gasparre et al. 2013). This evidence concerns the gene PPARGC1A and neoplasm.