In the particular context of CLL, the results of several studies have demonstrated that the TME can increase tumor cell survival by modulating tumor cells’ mitochondrial oxidative phosphorylation and nucleotide synthesis [20], favoring protection against oxidative stress by promoting glutathione synthesis [21] and causing a glycolytic switch through Notch-c-Myc signaling [22]. The gene discussed is MYC; the disease is neoplasm.