The emphasis of our approach is not to directly define the cis LOUREIRIN-B variants that underlie QTL but rather to understand how this variation drives changes in entire networks of genes that regulate physiological processes. For example, it is unclear from our analysis what the underlying perturbation on chromosome 8 that drive the trans8_eQTL signature are, but it is apparent that the genes whose expression traits map here in trans are the molecular effectors of the cis signal. We have shown this by demonstrating: a) that the adipose expression of genes in the trans8_eQTL signature is highly correlated with the adiposityrelated traits; b) that the genes test causal for driving variation in the adiposity traits; c) that the genes map to modules in human adipose that have been implicated in human obesity; and d) by validating three of the genes in the signature by phenotyping knockout mice. To explore the modular structures of the co-expression network, the adjacency matrix is further transformed into a topological overlap matrix. Topological overlap between two genes reflects not only their direct interaction but also their indirect interactions through all the other genes in the network, and previous studies have shown that topological overlap leads to more cohesive and biologically more meaningful modules. To identify modules of highly co-regulated genes, we used average linkage hierarchical clustering to group genes based on the topological overlap of their connectivity, followed by a dynamic cut-tree algorithm to dynamically cut clustering dendrogram branches into gene modules. 35 modules are identified and the module size, in number of genes, varies from 20 to 2,035. To distinguish between modules, each module was assigned a unique color identifier, with the remaining, poorly connected genes colored grey. Figure S10 shows the hierarchical clustering over the topological overlap matrix and the identified modules for the MCI BxA adipose. In this type of map, the rows and the columns represent genes in a symmetric fashion, and the color intensity represents the interaction strength between genes. This connectivity map highlights genes in the adipose transcriptional network that fall into distinct network modules, where genes within a given module are more interconnected with each other than with genes in other modules. The acquired capability to escape apoptosis is required at several steps during cancer development. Over-expression of the Benzethonium Chloride Bcl-xL protein is known to confer resistance to a broad range of potentially apoptotic stimuli arising during cancer development, such as oncogene activation, hypoxia and matrix detachment. Impaired apoptosis due to the over-expression of the Bcl-xL gene is therefore critical during cancer progression. Impaired apoptosis is also a major barrier to effective cancer treatment, because cytotoxic therapies for cancer strongly rely on induction of apoptosis. Interestingly, Bcl-xL has been suggested to play a unique role in general resistance to cytotoxic agents, because of a striking correlation between an increased Bcl-xL expression level and resistance to a wide panel of standard chemotherapy agents. Bcl-xL’s mechanism of action is therefore a major component of chemoresistance in cancer cells. Bcl-xL belongs to the Bcl-2 family of proteins whose members can have either anti-apoptotic or pro-apoptotic functions. The proapoptotic members of the Bcl2 family fall into two subsets. The so-called multidomain factors are proteins sharing more than one Bcl-2 Homology domain. The other subfamily comprises proteins sharing only the BH3 domain. A picture has emerged suggesting that ”BH3 only” proteins have diverse mechanisms of regulation and are targeted sensors of different 
sources of cell stress. Their primary function appears to be the binding and neutralization of the antiapoptotic Bcl-2 family membres, although some of them have also been reported to be able to directly activate multidomain proapoptotic family members. It is therefore widely accepted that because it increases the cellular potential to inactivate.