Although both metabolic disorders are activated by insulin depletion, diabetic ketoacidosis results from an absolute and usually abrupt drop of insulin delivery, while gliflozin‐related ketoacidosis depends on a slight reduction of insulin requirement due to amelioration in glucose control and reactive hyperglucagonemia as a braking system to glycosuria and consequent calorie loss by urine [106, 107]. The gene discussed is INS; the disease is type 2 diabetes mellitus.