Do these interchromosomal associations represent functional interactions, and if so what could drive the formation of these structures? It is conceivable that the results reflect the mingling observed for active loci at the regions between chromosomes. Indeed, transcription has been detected in these regions, and the recruitment of genomic regions on different chromosomes to a shared transcription factory could lead to the interchromosomal associations observed in 4Cv. This is consistent with the finding that distant active genes, on the same or even different chromosomes, can be found in proximity, possibly in transcription factories. 4C data suggest that chromosomes dynamically fold into transcriptionally active and inactive regions. The changes in nuclear localisation observed in FISH experiments could therefore be driven by changes in the occupancy of shared transcription factories. This is supported by the finding that inhibiting transcription alters the size and morphology of chromosome territory and regions of chromosome mingling, arguing that transcription in factories is a major driving force in the arrangement of chromosomes. The apparent relocation of the b-globin away from pericentric heterochromatin is preceded by transcriptional activation, suggesting that transcription may be required for the movement. Indeed, deletion of the LCR BYL719 prevents this change in nuclear organisation, though it remains to be determined if this is caused by a lack of transcription due to enhancer loss or a separable activity of the LCR. The interaction of distal genes, detected by 3C, appeared to depend on transcriptional initiation but not elongation. Results from 4C show that inhibition of transcription does not lead to a loss of the compartmentalised chromosome arrangement. Taken together these data suggest transcription is required to initiate, but not maintain, such structures. Our data also agree with the results of another 4C assay, showing that transcriptional induction of the HoxB1 gene in mouse cells led to a greater frequency of interchromosomal interaction. Thus, whilst our results argue for a model of increased mingling with other chromosomes associated with transcriptional activation it remains to be established if the structures of local gene clusters, chromosomes, and interchromosomal arrangements are maintained or established by transcription, and if these structures are functionally separable. Understanding the epigenetic regulation in human pluripotent stem cells, therefore, enable us to elucidate “stemness” and to screen for optimum iPS/ES cells for human therapeutic applications. Human extra-embryonic amnion cells are a useful cell source for generation of iPS cells, because they can be collected without invasion and are conventionally freezestorable. Recently, we generated iPS cells from human amnion cells as well as human fetal lung fibroblast cells. Here, we show DNA methylation profiles of human pluripotent stem cells including iPS cells, which were derived from extra-embryonic amnion cells and fetal lung fibroblast cells.