We have previously demonstrated that stabilization of HIF-1α is specifically necessary for alterations in cellular glucose metabolism, mitochondrial oxidative metabolism and mitochondrial abundance in Vhl-deficient and Vhl/Trp53-deficient renal epithelial cells in vivo [8], suggesting that these might be some of the cellular alterations that are required for tumour initiation. Here, HIF1A is linked to neoplasm.