KRAS and neoplasm: The expression levels of oncogenes (e.g. MYC [22, 100], mTOR [101] and KRAS [102]) and tumor suppressors (e.g. SIRT4 [103] and TP53 [104]) are decisive to regulate glutamine metabolism [92, 105], to the extent that tumor genetics can dictate cellular dependence on glutamine for survival [98].