In support of adipose tissue dysfunction as an early pathogenic event in the development of T2D, the authors reported that pre-diabetic states including impaired fasting glucose and impaired glucose tolerance are associated with increased concentrations of a range of inflammatory cytokines secreted from the adipose tissue, such as chemerin, fetuin-A and retinol binding protein 4 (RBP4) and a decrease in adiponectin, compared to NGT subjects. The gene discussed is AHSG; the disease is type 2 diabetes mellitus.