Neutrophil shells maintain structural and functional integrity during chemotaxis and migrate extensively to the tumor under the influence of chemokines, such as CXCL1 and CXCL2.[61] Stimulated by the inflammatory environment within the tumor, neutrophils release NETs, facilitating substantial accumulation of the chemotherapeutic drug DOX at the tumor site.[62] This approach exhibited outstanding therapeutic efficacy in a murine model of breast cancer, significantly delaying tumor growth. This evidence concerns the gene CXCL2 and breast cancer.