In contrast, in patients with T2D, glucose-dependency of GIP-stimulated glucagon secretion, such as in healthy people, does not remain (Figure 2).32 Elimination of GIPR activity in β-cells demonstrated a characteristic of T2D, associated with reduced postprandial insulin secretion and hyperglycaemia (Figure 2). The gene discussed is GIPR; the disease is type 2 diabetes mellitus.