The AKT1 overexpression in β-cells lead to increased islet mass [29], while the β-cell-specific Ir knockout (βIrKO) lead to reduced glucose-stimulated insulin secretion (GSIS), lower islet insulin content, and glucose intolerance, supporting the consensus that the loss of insulin action on β-cells leads to β-cell failure and T2DM [30]. The gene discussed is INS; the disease is Glucose intolerance.