A key observation in these presented results was the magnitude of hypermethylation in PC3 cells, which occurred at almost all of the inactive CpG island genes. A second key observation was that when PRC marks were depleted, a PC3 hypermethylation was observed. One possible model that can explain these observations assumes that DNA methylation in PC3 cells sweeps all CpGs that are not physically protected (or "masked") (Figure 3). According to this "passive" methylation model, transcription initiation complexes at the TSS [RNA PolII and related chromatin marks, can serve as one masking mechanism (Figure 3a), and Polycomb repressive complexes can serve as another (Figure 3b). This view was also supported by recent data on DNA methylation patterns of mouse ESCs. It is important to note that even if Polycomb complexes mask loci from de novo DNA methylation, it is possible that PRC activity (or recruitment) is not masked by DNA methylation (Figure 3c). This may be the case in some of the de novo PRC targets we ob more