CCR7 and neoplasm: It is striking that treatment with low dose of 2DG, an inhibitor of glycolysis and oxidative phosphorylation, induces metabolic reprogramming of BM-DCs in a similar manner as integrin deficiency.18 Importantly, this DC activation caused by metabolic restriction is reflected in increased DC-mediated tumor growth inhibition in vivo, presumably by affecting CCR7-dependent DC migration to lymph nodes and/or T cell activation, where IL-12 production plays a major role, or a combination of these effects.