An alternative explanation for the observed reduced expression of CXCR4 in metastatic as compared to therapy-naïve EWS lesions might be that the CXCR4-CXCL12 axis is essential for retention of EWS cells within the primary tumor site, as has been described for CD34+ hematopoietic stem cells and leukemic cells within the hematopoietic microenvironment[2] and, more recently, for osteosarcoma[29]. The gene discussed is CXCR4; the disease is neoplasm.