High rates of tumor cell glycolysis can activate the autophagy signaling pathway and AMP-activated protein kinase ULK1 (AMPK-ULK1), resulting in inhibition of enhancer-binding protein beta (CEBPB) subtypes and activation of liver-enriched activator protein (LAP), thus controlling the expression of GM-CSF and granulocyte colony-stimulating factor (G-CSF), supporting the formation of MDSCs, reducing the number of effector CD8+ T cells, weakening antitumor immunity, and hastening the progression of TNBC. This evidence concerns the gene CEBPB and neoplasm.