Since Lerner and Porte first provided compelling evidence pointing towards defective insulin storage and/or secretion in patients with T2D,21 β‐cell failure is acknowledged as the primary underlying cause of overt hyperglycaemia and T2D progression,20thus, there is now little doubt deficient insulin secretion in T2D results both from β‐cell dysfunction and β‐cell death.22, 23. The gene discussed is INS; the disease is Hyperglycemia.