This is highlighted by the high rate of diabetic ketoacidosis in the autoantibody-negative adults, possibly reflecting either previously proposed glucotoxicity-induced transient insulin deficiency [39] or the severe insulin-deficient subtype of type 2 diabetes proposed by Ahlqvist et al [40], who observed that 25% of this cluster had diabetic ketoacidosis at presentation. The gene discussed is INS; the disease is diabetic ketoacidosis.