PAX3- and PAX7-FKHR gene fusion [51], mutations in the von Hippel Lindau tumor suppressor gene [52], hypoxia in the tumor microenvironment [53], NF-κB [44], and inflammatory cytokines such as vascular endothelial growth factor [54] and tumor necrosis factor alpha [50], have all been implicated in CXCR4 overexpression. Here, FOXO1 is linked to neoplasm.