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The advancement of LUAD is influenced by the immune tumor microenvironment through paracrine signaling. However, the involvement of NKX2\u20101 in modeling the tumor immune microenvironment is still unclear. Here, the downregulation of NKX2\u20101 is observed in high\u2010grade LUAD. Meanwhile, single\u2010cell RNA sequencing and Visium in situ capturing profiling revealed the recruitment and infiltration of neutrophils in orthotopic syngeneic tumors exhibiting strong cell\u2010cell communication through the activation of CXCLs\/CXCR2 signaling. The depletion of NKX2\u20101 triggered the expression and secretion of CXCL1, CXCL2, CXCL3, and CXCL5 in LUAD cells. Chemokine secretion is analyzed by chemokine array and validated by qRT\u2010PCR. ATAC\u2010seq revealed the restrictive regulation of NKX2\u20101 on the promoters of\n                    <jats:italic>CXCL1<\/jats:italic>\n                    ,\n                    <jats:italic>CXCL2<\/jats:italic>\n                    , and\n                    <jats:italic>CXCL5<\/jats:italic>\n                    genes. This phenomenon led to increased tumor growth, and conversely, tumor growth decreased when inhibited by the CXCR2 antagonist SB225002. This study unveils how NKX2\u20101 modulates the infiltration of tumor\u2010promoting neutrophils by inhibiting CXCLs\/CXCR2\u2010dependent mechanisms. 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