Metastasis is the deadly face of epithelial tumors. The studies performed in the last decade have shed considerable light on the processes involved in the metastatic cascade. In particular, much effort has focused on defining the molecular changes that govern the conversion from an epithelial to a mesenchymal cell, a process known as epithelial-mesenchymal transition (EMT). The process of EMT is considered a fundamental event in the metastatic cascade (i.e. during invasion and/or intravasation) and several molecules involved in EMT have been described, including epithelial markers, transcription factors, as well as extracellular proteins and growth factors. In this green series article, we will focus our attention on the new molecules described in the recent years that appear to influence EMT and that are therefore relevant to epithelial carcinogenesis. Furthermore, we will try to explain how these molecules collaborate with the tumor microenvironment to trigger metastasis. Recent advances in our understanding of this process is generating a wide range of molecules that could be potentially considered as new therapeutic targets for drug design to block metastatic spreading.