Chronic stress triggers the formation of a previously unknown neutrophil subtype called cancer stress-primed (CSP) neutrophils, characterized by elevated expression of chemokines CCL3, CCL4, and CXCL2. These specialized immune cells actively recruit CCR1-positive breast cancer cells to the lungs through a corticosterone-mediated pathway involving the transcription factor CEBPB. This discovery fundamentally reframes how psychological stress influences cancer progression. Rather than simply weakening immune defenses, stress appears to actively reprogram neutrophils into metastasis-promoting agents that prepare the lung microenvironment for tumor colonization. The research provides compelling mechanistic evidence for the long-observed clinical correlation between chronic stress and poor cancer outcomes. Multiple therapeutic interventions targeting this pathway—including neutrophil depletion, chemokine knockout, and CCR1 inhibition—successfully reduced lung metastasis in mouse models. This suggests stress management could be more than supportive care for breast cancer patients; it might be a legitimate anti-metastatic strategy. However, the findings require validation in human studies, and the complexity of stress responses in clinical settings may differ significantly from controlled laboratory conditions. The work opens new avenues for both behavioral interventions and targeted therapies that could interrupt stress-driven metastatic cascades.