Significantly enriched in the human AN-survival genes, in genes that participate in human HCC network changes, and in genes associated in human HCC with sCNV. This is directly supports the hypothesis that the pre-tumor state, as measured by the AN tissue, was a significant determinant of the large scale network transformations required to produce HCC tumorigenesis. There are a number of interesting ideas that derive from this hypothesis. One is that MET overexpression causes increased tumorigenesis by altering the genes that participate in that transition, or in other words the starting state of these genes is causally related to the probability of the future transformation occurring. Similarly then, the starting state of the AN-survival genes may be causal for the probability of network transformations involving them in human HCC. The TU-survival genes in an analogous manner may also be causally related to the probability of future network evolutions relevant to disease progression. This further suggests, that as in the MET case, manipulation of the relevant genes will alter the probability of HCC network changes and tumor evolution occurring. The finding that AN-survival genes for the most part lose their predictive value in tumor is interesting. By implication once the network transformation has occurred those genes and their associated functions were generally no longer rate limiting. This is apparently largely true for both disruption of normal networks and creation of new networks. From a perspective of targeting tumors, disruption of normal networks may be hard to reverse in practice. However the creation of new networks may represent functions that the tumor has gained or emphasized relative to the tissue from which it was derived. As such these functions may make desirable targets in that the tumors have selected for them and the selection process may relate to survival. Targeting these new networks may therefore disrupt essential tumor specific functions. Finally, TU-survival genes may also represent an opportunity for intervention in that as described above they may causally relate to the probability of future disease progression. Investigation of coexpression networks highlighted 4 co-expression modules that were enriched for TU-survival genes. Two of the 4 modules were strongly linked to Gomisin-D ribosomes and ribosome biogenesis, which have been linked to aggressive disease in other tumor types and individual components when either over or under expressed promote tumorigenesis. Myc has been shown to alter a number of ribosome components and in turn can be regulated by them and was found here to be in the same co-expression network. This suggests that altered translation maybe a significant factor in HCC disease progression. A third co-expression module was unusually found to be enriched for both AN and TU-survival genes and centered around metabolism and the mitochondrion. Although it is speculation it is tempting to suggest that this group of genes may represent the molecular equivalent of the Orbifloxacin epidemiological observation that obesity is a risk factor for susceptibility to HCC and survival after diagnosis. Interestingly it was recently suggested that switching to a low fat diet alters the course of disease in mouse models. Gliomas are the most common primary brain tumors, characterized by the infiltration of neighboring brain structures and robust expansion during progression to a glioblastoma multiforme. Gliomas are frequently characterized by dysregulated signaling downstream of growth factor receptors such as EGFR, PDGFR, and IGFR, and elevated production of their corresponding ligands.