We also show that mimicking such metabolic stress in wild-type (WT) BM-DCs by treating cells with low concentration of glycolysis inhibitor, 2-deoxyglucose (2DG), drives increased DC activation (increased expression of IL-12 and CCR7, in vitro migration and T cell activation potential), increased H3K4me3 and H3K27me3 histone methylation, and enhanced anti-tumor responses in vivo. The gene discussed is CCR7; the disease is neoplasm.