“…The functional enrichment analysis indicated that the DEGs were primarily involved in the defense response, secretory vesicle, identical protein binding, cell adhesion, extracellular matrix, structural molecule activity, neutrophil degranulation and extracellular matrix organization. Neutrophil degranulation [52], innate immune system [53], platelet degranulation [54], extracellular matrix organization [55], diseases of glycosylation [56], platelet activation, signaling and aggregation [57], hemostasis [58], secretion [59], secretory vesicle [60], transmembrane transporter activity [61], cell adhesion [62], localization of cell [63], extracellular matrix [55], intrinsic component of plasma membrane [64], structural molecule activity [65], signaling receptor binding [66], have been highly noted in T2DM. Reports indicate that HIF1A [67], HLA-DRB1 [68], CHI3L1 [69], ADORA2A [70], ADRB2 [71], CLU (clusterin) [72], AGT (angiotensinogen) [73], VCAM1 [74], PPARA (peroxisome proliferator activated receptor alpha) [75], APOL1 [76], ZFP36 [77], PPM1B [78], SOCS1 [79], SNCA (synuclein alpha) [80], CTSS (cathepsin S) [81], IL6R [82], CFB (complement factor B) [83], DEFB1 [84], VNN1 [85], RAB27A [86], DPP4 [87], RARRES2 [88], CASP1 [89], LCN2 [90], REG3A [91], CD74 [92], PCSK2 [93], CHGB (chromogranin B) [94], TTR (transthyretin) [95], LRG1 [96], ALB (albumin) [97], DPP7 [98], APOH (apolipoprotein H) [99], CTSD (cathepsin D) [100], GCG (glucagon) [101], KCNQ1 [102], NR4A1 [103], PLIN5 [104], ALDH2 [105], ANG (angiogenin) [106], CLDN7 [107], PRLR (prolactin receptor) [108], SOD2 [109], MLXIPL (MLX interacting protein like) [110], CTSD (cathepsin D) [111], PECAM1 [112], ADA (adenosine deaminase) [113], MFGE8 […”