Although we did not experimentally examine downstream signaling pathways in our models, prior preclinical and translational studies indicate that G-CSF can activate pro-survival signaling pathways (STAT3 and PI3K/AKT), induce the epithelial–mesenchymal transition (EMT), and expand myeloid-derived suppressor cells, thereby fostering an immunosuppressive tumor microenvironment [19]. The gene discussed is STAT3; the disease is neoplasm.