In lung cancer, the activation of neutrophils in the TME introduces complexity to the inflamed environment by triggering additional mechanisms.[27] Our observations indicate that the downregulation of NKX2‐1 promotes the recruitment and infiltration of neutrophils into LUAD tumors through the secretion of chemokines such as CXCL1, CXCL2, CXCL3, and CXCL5 into the TME (Figure 2, 3, 4), further fostering tumor‐promoting effects (Figure 6 and 7). Here, NKX2-1 is linked to neoplasm.