In a mouse tumor model, it was shown that radiation therapy triggers the secretion of CXCL1, CXCL2, and CCL5, which leads to neutrophil recruitment to tumor sites; in turn, neutrophils generate ROS and suppress PI3K/AKT/SNAI1 signaling, inhibiting epithelial–mesenchymal transition [94]. The gene discussed is CXCL1; the disease is neoplasm.