lial cells, and sensory neurons [4]. Evidence indicates that Gal-3 overexpression in retina tissue [5, 6] and RPE cells [4] participates in the pathogenesis of DR. Gal-3 can be detected in circulation, and its level was found to be positively correlated with obesity, insulin resistance, DM, diabetic macrovascular complications, and diabetic nephropathy [7][8][9][10][11]. However, data about circulating Gal-3 levels and DR are limited.Fetuin-A (Fet-A) is a 64-kDa heterodimeric glycoprotein produced by the adipose tissue and liver [12]. Evidence indicates that circulating Fet-A is positively associated with insulin resistance, obesity, and T2DM [3]. Moreover, Fet-A was also found to stimulate pro-angiogenic factors, such as vascular endothelial growth factor (VEGF) [13][14][15]. Thus, the Fet-A level could be an early initiator of DR [13]. However, the cor-