In triple-negative BC mouse models, glycolytic metabolism may repress specific CCAAT/enhancer-binding protein beta (CEBPB) isoforms and liver-enriched activator protein (LAP) via AMP-activated protein kinase (AMPK)-ULK1 and autophagic pathways to effectively stimulate tumor G-CSF and GM-CSF expression and to maintain MDSCs development and escape immunity [128]. The gene discussed is CSF3; the disease is neoplasm.