It is only recently that advances in stem cell biology generated the experimental framework necessary to test this Reya et al., 2001; Sell et al., 2004). According to the cancer stem cell model, tumors originate in either tissue stem cells or progenitor cells, through deregulation of the normally tightly regulated process of self-renewal (Molofsky et al., 2004; Passegue et al., 2003). Self-renewal is the process by which stem cells generate progeny identical to themselves. Stem cells also differentiate to generate multipotent progenitors, which in turn give rise to committed progenitors and differentiated cells. Cancer stem cells share these properties with their normal counterparts: they have self-renewal capacity, driving tumorigenicity, recurrence and metastasis and they have the capacity to differentiate, albeit aberrantly, giving rise to a heterogeneous population of cancer cells. The differentiated cells constitute the bulk of the tumor, but they are not tumorigenic, due to their lack of self-renewal capacity and limited proliferation potential.