Endothelial stem cells are one of three types of multipotent stem cells found in bone marrow. They give rise to progenitor cells, which are intermediate stem cells that lose potency, and eventually produce endothelial cells, which create the thin-walled endothelium that lines the inner surface of blood vessels and lymphatic vessels. The epithelial–mesenchymal transition (EMT) is a process by which epithelial cells lose their cell polarity and cell–cell adhesion and gain migratory and invasive properties to become mesenchymal stem cells; these are multipotent stromal cells that can differentiate into a variety of cell types. EMT is essential for numerous developmental processes, including mesoderm, neural tube formation, and wound healing. A growing body of evidence suggests that EMT plays a central role during tumor metastasis and frequently imparts a stem cell-like phenotype and therapeutic resistance to tumor cells. The induction of EMT is accompanied by a dynamic reprogramming of the epigenome involving changes in DNA methylation and several post-translational histone modifications. These changes in turn promote the expression of mesenchymal genes or repress those associated with an epithelial phenotype. EMT of cancer cells is partly under reversible epigenetic control [36]. Differences between cell types are guided by the expression of tissue-specific transcription factors and consolidation of associated epigenetic states. Therefore, the epigenome of a cancer cell is determined in part by the cell of origin for that cancer and includes passenger hypermethylation events at genes not required in that particular lineage