In the June 4th issue of Cell Stem Cell, A. P. Aiden et al. from Harvard University reported their study results on identifying transcriptional and epigenetic mechanisms which give rise to Wilms tumor formation. With a comparison of genome-wide chromatin profiling of cells derived from Wilms tumors, embryonic stem cells (ESCs), and normal kidney, the investigators found that large active chromatin domains normally regulating gene expression in ESCs were also expressed in Wilms cells. These genes were associated with kidney development as well as maintaining the adult renal stem cell compartment. Interestingly, the Wilms cells expressing the embryonic-like chromatin regulators maintain stem cells in the kidney compartment by silencing p16. The experimental data revealed that these "bivalent promoters" in Wilms tumor correlated to silencing genes during early stages of differentiation in kidney progenitors. The authors concluded from their experimental results which they suggest that "Wilms cells share a transcriptional and epigenetic landscape with normal renal stem cells, which is inherently susceptible to transformation and my represent a cell of origin for this disease" (i.e. cancer stem cells).