In the context of human Ewing sarcoma, knockdown of HOXD10, HOXD11, and HOXD13 all independently impaired the growth and invasive properties of tumor cells, demonstrating that despite the marked over-expression of HOXD13, all members of the posterior HOXD cluster contribute to human tumorigenesis [18]. This evidence concerns the gene HOXD11 and neoplasm.