CXCR4 and neoplasm: Vascular injury and perfusion heterogeneity generate and maintain hypoxia, stabilizing HIF‐1α and transcriptional programs that upregulate VEGF and CXCL12, thereby promoting angiogenic rebound and recruitment of CXCR4+ bone‐marrow–derived cells after RT—processes linked to radioresistance and tumor regrowth [112].