## 1 Introduction  
Type 2 diabetes mellitus (T2 DM) is a chronic metabolic disease that can significantly impact daily life and result in severe complications. It is characterized by elevated levels of plasma glucose due to impaired glucose metabolism, insulin resistance, and impaired insulin secretion. The dysregulation of glucose homeostasis, leading to T2 DM, can be attributed to various mechanisms such as reduced peripheral glucose uptake in muscles, cytokine secretion in adipose tissue, increased glucose production in the liver, impaired insulin secretion in the pancreas, and neuroendocrine regulation by the central nervous system [1]. Hyperglycemia, a hallmark of T2 DM, can lead to the overproduction of reactive oxygen species (ROS), causing oxidative stress and redox imbalance, which is a major contributor to the etiology of T2 DM [2]. Extensive research efforts have been directed towards understanding the genetic susceptibility to T2 DM. In particular, genome-wide association studies (GWAS) have been extensively conducted over the past 15 years, moving away from the limited scope of linkage analysis that only identified genetic variants segregating within families. These GWAS studies have made significant contributions to the identification of common genetic factors associated with T2 DM. The findings from these studies provide valuable insights into the pathological pathways involved in the development of T2 DM. For instance, rs13266634,previously identified in studies by [PERSON] et al. [3], [PERSON] et al. [4], and [PERSON] et al. [5], is an exonic variant of SLC30A8. This variant creates an R to W missense mutation at position 325 in the \(\beta\)-cell zinc transporter ZnT-8, which plays a crucial role in the final biosynthetic pathway of insulin production and secretion [6; 7]. However, the precise contributions of many GWAS signals to T2 DM susceptibility remain unclear, as they are often located in intergenic regions, and their target genes are assigned physically close to these signals. To address this challenge, researchers have explored expression quantitative trait loci (eQTLs) and their corresponding target genes (eGenes). An example of this approach is the identification of 33 eGenes through the integration of 143 meta-GWAS signals with gene expression data from blood samples [8]. Nonetheless, our understanding of the functional roles of eGenes remains limited, as their association with T2 DM does not necessarily indicate that a particular tissue is implicated in T2 DM development. Recent eQTL studies have focused on tissue-specific eQTL-eGene associations. For instance, a study examining eQTLs specific to skeletal muscle revealed an eQTL (rs4547172; \(p<\) 1.96 \(\times\) 10\({}^{-5}\)) of _PFKM_, a critical regulatory enzyme of glycolysis [9]. This eQTL was found to be in linkage with a T2 DM GWAS signal (rs11168327; \(p=\) 2.7 \(\times\) 10\({}^{-3}\)) identified by the DIAGRAM consortium [10]. Furthermore, based on the additional association of this eQTL with glucose uptake in skeletal muscle (\(p=\) 0.016), _PFKM_ has been proposed as a potential factor involved in the regulation of insulin sensitivity in skeletal muscle cells. Another association study of T2 DM with genes encoding glutathione-metabolizing enzymes (GSS and GGT7) identified nucleotide variants (rs13041792, rs6119534, and rs11546155; \(p<\) 0.05) in linkage to eQTLs associated (\(p<\) 0.05) with the pancreatic expression of genes (MAP1 LC3A, EDEM2, MYH7B, and CPNE1) involved in the unfolded protein response pathway [11]. This study suggests a hypothesis that glutathione deficiency may contribute to misfolded proinsulin, leading to apoptosis of pancreatic beta cells. Other tissue-specific eQTL studies have indicated additional etiological factors in T2 DM, such as metabolic stress-induced beta cell dysfunction [12] and mitochondrial dysfunction in adipose tissue [13].