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From the triumvirate to the ominous octet and beyond, the pathophysiology of type 2 diabetes (T2D) has been progressively expanded to integrate an increasingly complex network of metabolic abnormalities.1 Nevertheless, despite these advances and the recognition of numerous additional contributors to dysglycemia, our conceptual framework for T2D in 2026 still rests on two fundamental defects: insulin resistance and progressive β-cell dysfunction. These abnormalities have shaped both our understanding of disease progression and the development of modern glucose-lowering therapies. Yet despite major advances in diabetes care, an important physiological question remains unresolved: why does glucagon secretion remain inappropriately elevated even in the presence of hyperglycemia and hyperinsulinemia?1