Type 2 diabetes is characterized by insulin resistance and a progressive loss of β‐cell function induced by a combination of both β‐cell loss and impaired insulin secretion from remaining β‐cells. Here, we review the fate of the β‐cell under chronic hyperglycaemic conditions with regard to β‐cell mass, gene expression, hormone content, secretory capacity and the ability to de‐ or transdifferentiate into other cell types. We compare data from various in vivo and in vitro models of diabetes with a novel mouse model of inducible, reversible hyperglycaemia (βV59M mice). We suggest that insulin staining using standard histological methods may not always provide an accurate estimation of β‐cell mass or number. We consider how β‐cell identity is best defined, and whether expression of transcription factors normally found in islet progenitor cells, or in α‐cells, implies that mature β‐cells have undergone dedifferentiation or transdifferentiation. We propose that even in long‐standing diabetes, β‐cells predominantly remain β‐cells—but not as we know them.