In addition, we found the induction of the Defensin gene: DEFA1/HNP-1 which was also up-regulated in both RA andT2D in the current study. DEGsDEFA1/4 was a member of the family of microbicidal and cytotoxic peptides involved in host defense Sorafenib associated with RA. It is reported that up-regulation of human DEFA1mRNA in bone marrow-derived mononuclear cells is associated with rheumatoid arthritis in human. And others found that DEFA had a significantly higher expression in RA patients than in healthy controls from total RNA of PBMC. However, we did not find reports about the role that DEFA plays in the pathological process of T2D.Inour study, DEFA1/4 was up-regulated both in RA and T2D, involved in IL-8 signaling. This phenomenon revealed that DEFA1 might be a novel gene in T2D patients, and could be a potential biomarker in both RA and T2D. Except of agranulocyte adhesion and diapedesis pathways, MMP9 was also up-regulated in both the RA and theT2Dgroups involved inIL-8signaling, which can lead to an inflammatory response IWP-L6 through the regulation of endothelial cell migration during angiogenesis. In this point, we speculated that the up-regulated MMP9 involved in cytokine and cellular immune response signaling maybe theaetiopathogenesis commonality of RA and T2D. Furthermore, we know IL-1�� perpetuate Th17responses and endothelial cell damage, which potentiate therheumatoidarthritis.IL-1�� has important roles in endocrinology and in the regulation of responses associated with inflammatory stress. IL-1impairs insulin secretion and induces ��-cell apoptosis leading toT2D.IL-8 is strongly dependent of IL-1 beta and the level of IL-1 beta in RA and T2D remained unchanged in our study. It is elevated in other tissues and maybe the cause of the increase in IL-8 in the circulating immune cells. For the two shared pathways: natural killer cell signaling and differential regulation of cytokine production in intestinal epithelial cells by IL-17A and IL-17F, they were also found in both RA and T2D. Natural killer cells are large granular lymphocytes that are important to the innate immune system, which have the capacity to damage normal cells or through interaction with other cells such as dendritic cells, macrophages, and T cells cause autoimmune diseases, such as RA.