Moreover, in inducible genetic mouse models, we further showed that induction of BRSK2 expression in mature β cells caused persistent hyperinsulinemia, insulin resistance, and GSIS disability, while β-cell-specific Brsk2 deletion prevented mice from HFD-induced obesity and glucose intolerance through preserved GSIS function and favorable insulin sensitivity. The gene discussed is INS; the disease is obesity due to melanocortin 4 receptor deficiency.