Moreover, fluctuations in EWS-FLI1 levels are not the only mechanism known to initiate EwS dissemination51, and several candidates such as chemokine receptor CXCR4 signalling52, chromatin modifiers53, cadherins54, micro-RNAs55 and interactions with the tumour microenvironment including glucocorticoids56,57 have been proposed. The gene discussed is CXCR4; the disease is neoplasm.