A growing body of evidence indicates that the dysregulation of expression of non-coding RNA, particularly those involved in insulin secretion and glucose and lipid metabolism, can contribute to T2D development [201,202], while histone modifications appear to be involved in the pathophysiology of T2D, affecting the development of pancreatic β cells and insulin release, and complications of T2D [203,204]. This evidence concerns the gene INS and type 2 diabetes mellitus.