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. This evidence concerns the gene BRSK2 and obesity due to melanocortin 4 receptor deficiency.