Moreover, we demonstrated that blocking of CXCLs–CXCR2 axis in vivo induces tumor cell apoptosis with a shift of infiltrated immune-inflammatory cells in the PDAC lesions, as evidenced by reduced infiltration of neutrophils/MDSCs and arginase-1-positive macrophages, and increased inducible nitric oxide synthase (iNOS)-positive macrophages, leading to significant survival extension of PDAC-bearing mice. Here, CXCR2 is linked to neoplasm.