Type 1 diabetes (T1D) is caused by a loss of tolerance of the immune system (autoimmunity) to the body's own insulin-producing β cells of the pancreas, leading to their dysfunction and/or destruction resulting in insulin deficiency and hyperglycaemia.1 Autoreactive effector T lymphocytes (Teffs) are central to disease pathogenesis and it is thought that many cases of T1D are caused by poor regulation of Teffs by CD4+ FOXP3+ T regulatory cells (Tregs).2 The degree of β-cell destruction and insulin deficiency depends on the age of patients at diagnosis and the duration of their disease. This evidence concerns the gene INS and type 1 diabetes mellitus.