On the one hand, in HLRCC cell lines, it was shown that the glycolytic shift occurring in FH-deficient cells and HLRCC tumours leads to the inactivation of AMPK, and the activation of anabolic factors, acetyl-CoA carboxylase and ribosomal protein S6 (effector of the mammalian target of rapamycin-mTOR), that potentially could promote oncogenic growth in renal cancer [79]. This evidence concerns the gene MTOR and neoplasm.