In a triple-negative breast cancer model, tumour cells coordinate AMP-activated protein kinase (AMPK)-ULK1, autophagy, and CCAAT/enhancer-binding protein beta (CEBPB) molecular network via aerobic glycolysis to promote the secretion of granulocyte colony-stimulating factor (G-CSF) and granulocyte macrophage colony-stimulating factor (GM-CSF), and to maintain the growth and development of MDSCs to evade tumour immunity (150). The gene discussed is CEBPB; the disease is neoplasm.