This effect is due in part to the inability of exogenous insulin to mimic the normal profile of endogenous insulin production, leading to relative insulin excess at inappropriate times [2], impairment of the normal compensatory hormone responses to lower blood glucose [5] and the loss of behavioural responses due to IAH [2] which affects 20–40% of people with T1D [6,7]. This evidence concerns the gene INS and type 1 diabetes mellitus.