Among the most hazardous conditions affecting human health is diabetes mellitus (DM). Type 2 diabetes (T2DM) is the most prevalent type and represents about 90% of all diabetic cases globally and this form is characterized by hyperglycemia, which results from insulin resistance or inadequate insulin production. The severity of this metabolic disorder is attributed to its microvascular and macrovascular complications. In this study, in silico analysis was used to define the most putative pathways implicated in the occurrence and progression of T2DM by using bioinformatics tools as GEO2R to identify differential expression of genes (DEGs), Shiny Go 0.8 web program to identify gene-ontology (GO) terms and Kyoto- Encyclopedia of genes and genomes (KEGG) pathways, STRING database to determine protein-protein interaction, and Cytoscape software to visualize this interaction and to identify hub genes. The results showed that hub genes that regulate the pathogenesis of T2DM are Signal-transducer-and activator of transcription three (Stat3), discs large homolog 4(Dlg4), carnitine palmitoyltransferase 1 (Cpt1a), aldehyde dehydrogenase- 1- family member A1 (Aldh1a1), galectin 3) Lgals3(, integrin subunit alpha D) Itgad(, epoxide hydrolase 2) Ephx2(, colony stimulating factor 1 receptor) Csf1r(, transferrin receptor) Tfrc(, UDP glucuronosyltransferase 2 family, and polypeptide B1 )Ugt2b1(. Additionally, the most implicated pathway is the peroxisome proliferator-activated receptors (PPAR) signaling pathway. Finally, we can modulate T2DM progression by targeting STAT3 pathway and PPAR signaling pathway.