Moreover, our results on the hierarchical organization of neural networks suggest that the critical period for implementing this network organization could be the early phase of network formation. Indeed, our results originally demonstrate that once this organization is set it is preserved all along the developmental frame. Radiation induced genomic instability is a delayed, persistent effect of ionizing radiation exposure that manifests in the unirradiated progeny of irradiated cells as an increased frequency of mitotically heritable genetic alterations. Radiation induced genomic instability is a non-targeted phenomenon that is thought to contribute to radiation carcinogenesis, however the mechanisms underlying this process are poorly understood. The spectrum of alterations observed in cells exhibiting genomic instability include DNA double strand breaks, mutations, changes in gene expression, disruption of mitochondrial processes, chromosomal rearrangements, cell cycle arrest, and apoptotic cell death. Studies from a number of laboratories have attempted to elucidate the mechanisms that underlie the initiation and/or perpetuation of genomic instability. Based on such studies, many different mechanisms have been invoked, including persistent oxidative stress, mitochondrial dysfunction, increased cytokine secretion, and epigenetics. However, none of these mechanisms alone seem to be sufficient to induce genomic instability, suggesting that radiation induced genomic instability is a multifactorial phenomenon. Epigenetic mechanisms include altered DNA methylation, histone and chromatin modifications, and microRNA all of which can affect gene expression and cellular phenotype. Epigenetic aberrations have been observed following irradiation and also play a role in carcinogenic processes. In cancer cells, global hypomethylation can lead to the initiation of genomic instability. In MK-4827 PARP inhibitor particular hypomethylation of repeat elements, including long interspersed nuclear elements 1 and Alu elements, can lead to chromosomal instability, translocations, and gene disruption caused by the reactivation of transposable DNA sequences. In addition, transcriptional silencing of tumor suppressor genes can occur due to promoter hypermethylation and oncogene activation can occur due to promoter hypomethylation. MiR expression also plays an important role in the regulation of cellular pathways including cell proliferation, differentiation, and apoptosis by modulating gene expression. Deregulation of miR expression can result in disruption of these cellular pathways, contributing to carcinogenesis. Certain miR such as miR-34c, have also been shown to be involved in the control of genomic instability. Similarly, changes to histone marks and chromatin conformation can aberrantly alter gene expression and cellular phenotype and are associated with carcinogenesis.