Overall, we found that in the progression from NGT to IGT to type 2 diabetes the individual islets displayed: (1) a progressive decrease in markers associated with beta cell identity, together with chaperones and oxidoreductase factors; (2) a progressive increase in ER stress marker genes; (3) an increase in insulin processing machinery components in IGT islets as an attempt to compensate for the increase in insulin demand; (4) a progressive increase of altered in situ proinsulin expression and intracellular localisation. This evidence concerns the gene INS and type 2 diabetes mellitus.