This switch was associated with downregulation of the angiogenesis inhibitor thrombospondin and upregulation of genes not hitherto linked to tumor dormancy, such as endothelial cell-specific molecule 1 (ESM1), 5'-ectonucleotidase, tissue inhibitor of metalloproteinase 3 (TIMP3), epidermal growth factor receptor (EGFR), insulin-like growth factor receptor (IGF1R), phosphatidylinositol 3-kinase (PI3K) signaling, Eph receptor A5 (EphA5), and histone H2BK (206). This evidence concerns the gene EPHA5 and neoplasm.