OSM has been shown to function in breast and various other cancer cells in culture to (1) promote an epithelial-to-mesenchymal transition (EMT) and a stem cell-like phenotype [14, 20]; (2) upregulate expression of proteases such as matrix metalloproteinases [21]; (3) promote tumor cell detachment and subsequent invasion [22, 23]; (4) induce the expression of VEGF, hypoxia inducible factor-1α, and other proangiogenic factors [24]; and (5) suppress estrogen receptor (ER)-α expression [16]. This evidence concerns the gene ESR1 and neoplasm.