Similarly, after blocking downstream G-CSF signaling using STAT3 inhibitor LLL12, we observed partial restoration of neutrophil properties, namely inhibited neutrophil degranulation and lower accumulation of CD62Llow cells, confirming the key role of G-CSF/ G-CSFR axis in the tumor-induced dysregulation of neutrophil maturation and functions (Fig. S15). The gene discussed is STAT3; the disease is neoplasm.