Type 2 diabetes (T2D) is one of the major and exacer- bating health problems worldwide; T2D is predicted to affect 490 million in 2030 (Zhang, et al., 2010). Strong genetic in uences and many polymorphisms have been reproducibly associated with T2D.Insulin resistance in muscle, liver, and adipose tissues is a primary charac- teristic of most patients with T2D; as such, these tissues become resistant to endogenous and exogenous insulin. The interaction of insulin with target tissues is mediated by insulin receptor (INSR), a glycoprotein implicated in directing insulin to target cells and initiating cell responses to insulin, (Gold ne, 1987 Herder and Roden, 2011, Voight, et al., 2010). High-mobility group A1 (HMGA1) is an architectural transcription factor involved in numerous biological functions in the nucleus, including regulation of DNA replication, transcription, recombination, and repair; among these functions, transcriptional regulation of gene expression is considered as the most important. After HMGA1 binds to DNA, HMGA1 can be polymerized with other transcription factors, forming an “enhanceo- some†to regulate gene transcription; thus, gene expres- sions are positively or negatively regulated(Bustin and Reeves, 1996). Studies on humans and knockout mice have suggested that HMGA1 is involved in to T2D patho- genesis through the regulation of INSR gene expres- sion; INSR gene expression is decreased by functional HMGA1 gene variants. HMGA1-de cient patients have been biologically investigated because of their clinical value. However, whether HMGA1 single gene deletion- or mutation-induced insulin resistance is the underlying cause of T2D remains unknown, (Foti, et al., 2005). Low- frequency insertion polymorphism IVS5-13insC (c.136- 14_136-13insC) has been identi ed and associated with insulin resistance and T2D among individuals of white European ancestry and Chinese populations, (Chiefari, et al., 2011 Liu, et al., 2012)