At a genome-wide scale and thus for identifying regulatory pathways affecting disease susceptibility. For the analysis of mechanisms of gene regulation, the question of tissue dependency and specificity is of major relevance. In particular, expression patterns of disease-relevant tissues might further advance our understanding of disease pathophysiology. However, for ethical and practical reasons, eQTL analyses are often only feasible in whole blood rather than in disease-relevant tissues, particularly in large population based observational studies. Therefore, it is important to assess, whether regulation of gene expression in whole blood is robust and reflects gene expression patterns in other tissues or cell lines. In the past, eQTL mapping studies in whole blood have focused on genetic variation with an impact on gene regulation acting in trans to identify downstream mechanisms of these variants on clinical phenotypes or were restricted in sample size. In a previous work conducted in 322 European subjects, we found that whole blood eQTLs with effects in cis were reproducible, while the power to address this question for eQTLs with effects in trans was limited due to the burden of multiple testing. For that reason, here, we used a larger, distinct discovery sample and investigated data of 890 participants of the Cooperative Health Research in the Region of Augsburg F4 and 1,818 participants of two replication samples. Furthermore, up to now, it is unclear whether the study design or technical issues such as time of blood collection or usage of distinct laboratory tools have an impact on the reproducibility of results. These factors might be important as for example gene expression profiles in whole blood cell samples obtained using different laboratory reagents and protocols had been found to differ to large extents with the result of recommendations not to use them for joint or meta-analysis. Interleukin-7 is a potent T cell activating cytokine that causes proliferation, survival and differentiation of T cells in the periphery to maintain homeostatic T cell balance. Not only in health, but also in disease, IL-7 has been shown to play an important role in T cell expansion and enhancement of T celldriven immunity. Addition of IL-7 increases T cell numbers and functionality in immunodeficient states due to HIV infection, chemotherapy, and after bone marrow transplantation. Furthermore, IL-7 and its receptor have been implicated in Vorinostat several autoimmune diseases like rheumatoid arthritis, psoriasis, spondylarthritis, inflammatory bowel’s disease multiple sclerosis, and recently primary Syndrome. In the inflamed tissues of patients with autoimmune diseases, increased IL-7 production and IL-7 receptor expression by tissue cells and immune cells have been documented. In many in vitro models IL-7 was shown to induce T cell activation and T cell-dependent activation of monocytes/macrophages and dendritic.