As HDAC inhibitor treatment resulted in depletion of the myf5:GFP+/mylz2:mCherry−tumor cell subpopulation, which contains the tumor propagating cells with the capacity for self-renewal [17, 18], we next assessed the effect of HDAC inhibitors on the self-renewal capacity of ERMS in vivo by limiting dilution experiments. This evidence concerns the gene HDAC9 and neoplasm.