The predominant MODY subtypes are as follows: GCK-MODY, resulting in a high glycaemia set-point that typically should not be treated as it is not associated with microvascular complications of diabetes, and HNF1A- and HNF4A-MODY, which reduce glucose-mediated insulin secretion leading to progressive hyperglycaemia and complications, but with exquisite sulphonylurea sensitivity that often obviates the need for insulin [2]. This evidence concerns the gene INS and MODY.