Further studies have found that this reaction is related to PKM2 binding to mitofusion2 (MFN2), a key regulatory protein of mitochondrial fusion.[34] In addition, mTOR phosphorylates MFN2 to increase PKM2-MFN2 binding, thereby affecting PKM2-MFN2’s modulation of glycolysis, mitochondrial fusion, and OXPHOS.[34] Therefore, the mTOR-MFN2-PKM2 signaling axis regulates tumor cell growth by coupling glycolysis and OXPHOS. This evidence concerns the gene MFN2 and neoplasm.