What really causes type 2 diabetes? The best available information suggests that onset of type 2 diabetes is determined by relatively sudden failure of the beta cell to respond normally to a rise in blood glucose. Once established, the disease seems to behave as inevitably progressive with an irreversible beta cell defect. Certainly all the large studies of type 2 diabetes show a dismally progressive pattern such that around 50% of people require insulin therapy within 10 years. A variety of disease processes involving the pancreatic islets have been proposed to account for this, including amyloid deposition, oxidative stress and cytokine action. Where does insulin resistance fit in? It has seemed to be rather complicated. Several recent pieces of information appear not to fit with this complex analysis. When people lose weight due to any cause, blood glucose levels return towards normal even when insulin or oral agents are stopped. By developing new methodology to measure fat content in specific organs it has been possible to answer these questions, and to demonstrate the basic simplicity of mechanisms underlying type 2 diabetes. Normal beta cell function can be restored by weight loss alone, and observation on individuals for up to 9 years confirms durability. The implications for people with diabetes are considerable. However, this does not mean that type 2 diabetes is caused by obesity. Less than half of newly diagnosed people with type 2 diabetes have a BMI over 30kg/m2, and around 1 in 7 have a normal BMI. But for any one individual it appears that there is a threshold effect. If a person has more fat on board than he or she can store safely in the inert subcutaneous depot then type 2 diabetes will develop irrespective of BMI. Understanding what happens in one person is not well described by the population metric of BMI.