CXCL3 is a C-X-C chemokine that functions primarily as a neutrophil chemoattractant through CXCR2 receptor binding 1. The processed form GRO-gamma(5-73) exhibits enhanced chemotactic activity for neutrophilic granulocytes, and CXCL3 exerts effects on endothelial cells in autocrine fashion. Mechanistically, CXCL3 expression is regulated by multiple pathways: the JAK2/STAT3 pathway in colorectal cancer 2, the KRAS-IRF2 axis in colorectal cancer 3, NKX2-1 suppression in lung adenocarcinoma 4, and PDGF receptor signaling in gastric cancer 5. CXCL3 recruits myeloid-derived suppressor cells (MDSCs) and neutrophils to tumor microenvironments via CXCR2 signaling. In disease contexts, elevated CXCL3 correlates with poor prognosis in pancreatic cancer 6 and colorectal cancer 2. CXCL3 promotes cancer progression through multiple mechanisms: orchestrating neutrophil extracellular traps in aortic dissection 1, facilitating pancreatic cancer metastasis through myofibroblast transition 6, accumulating immunosuppressive PMN-MDSCs in colorectal cancer 2, and inducing ferroptotic neutrophils that suppress antitumor immunity in breast cancer 7. In rheumatoid arthritis, CXCL3 is upregulated in synovial macrophages via NF-κB signaling 8. Clinically, CXCR2 antagonism or CXCL3 blockade restores anti-PD-1 immunotherapy responsiveness and reduces tumor progression across multiple cancer types.