Research has shown that Myc, a prominent regulator of metabolic processes, induces genes that coordinate glucose and amino acid catabolism and control nutrient and metabolite transport in Eμ-Myc mice, contributing to the advancement of DLBCL.[22] Functional mutations in TP53 can affect glucose metabolism, which promotes DLBCL progression by activating glucose transporter protein (GLUT), glutaminase and fructose 2,6-bisphosphatase, inducing a metabolic shift to aerobic glycolysis and free radical generation[23] (Fig. 1). This evidence concerns the gene GLS and diffuse large B-cell lymphoma.