We found that only among the participants with lower genetic risk of lipodystrophy, the association between MSAB and the increased risk of developing T2D attuned, and other genetic risk in terms of β-cell function, proinsulin synthesis, obesity, liver function, and HbA1c deposition did not have such modification effects. The gene discussed is INS; the disease is obesity due to melanocortin 4 receptor deficiency.