Abnormal chemokine secretion in the tumor microenvironment disrupts these gradients; for example, CCR2/CCL2 and CXCR2/CXCL1 recruit immunosuppressive cells such as myeloid-derived suppressor cells, tumor-associated macrophages, and neutrophils, promoting abnormal vascularization and physically isolating neoantigen-specific TILs (80). The gene discussed is CXCL1; the disease is neoplasm.