In addition to directly promoting the anti-tumor pro-inflammatory phenotype of neutrophils, our findings suggested that the ferroptosis-activated neutrophils could further promote T-cell infiltration via secreting CXCL9, CXCL10, and CXCL11 and enhance Th1 differentiation via secreting IL12A and IL12B in the TME. Here, CXCL9 is linked to neoplasm.