Tumor cell glycolysis, through molecular networks such as AMPK-ULK1, autophagy, and the enhancer binding protein beta (CEBPB) pathway, inhibits the expression of tumor granulocyte colony-stimulating factor (G-CSF) and granulocyte-macrophage colony-stimulating factor (GM-CSF) expression, thereby promoting the proliferation of MDSCs and maintaining tumor immunosuppression (Li et al., 2018). This evidence concerns the gene ULK1 and neoplasm.