<i>In vitro</i> experiments show that CAMP promotes malignant proliferation and activates inflammatory pathways in cervical cancer, whereas RCT suppresses these effects and modulates the COL1A1/COL1A2-CD44 and ANXA1-FPR1/FPR2 axes, reshaping tumor microenvironmental adhesion and immune activity.<h4>Conclusion</h4>CAMP is a key regulator of neutrophil differentiation and tumor immune microenvironment remodeling in cervical cancer and during RCT. The gene discussed is FPR1; the disease is cervical cancer.