For example, nuclear translocation of NF-κB drives transcription of a gene encoding a scaffold that allows AKT phosphorylation to increase GLUT1 localization to the plasma membrane, while tumor protein P53 (TP53), MYC and hypoxia-inducible factor-1α (HIF-1α) upregulate the expression levels of GLUTs and thus lead to greater glycolytic flux in DLBCL [31,32]. Here, NFKB1 is linked to diffuse large B-cell lymphoma.