In vitro experiments verified that SGLT-2 inhibitors ameliorated obesity by increasing glucose uptake in skeletal muscle and lipolysis in adipose tissue; consequently, blood ketone levels in the SGLT-2 inhibitor group were raised.[14,15] Under normal circumstances, the induction of ketosis by SGLT-2 inhibitors is precluded due to the regulatory feedback mechanisms in the human body.[16,17] However, during conditions of fasting, surgery, acute infection, or insulin deprivation, the occurrence of DKA is markedly augmented.[18]. The gene discussed is INS; the disease is obesity disorder.