Taking into account that individuals after an attack of pancreatitis have significantly higher intra-pancreatic fat deposition compared with healthy controls [66] and given the findings of significant inverse associations of intra-pancreatic fat deposition and indices of insulin sensitivity in non-obese NODAP individuals (but not in T2DM) [67], leptin could be a potential driver of glucose metabolism abnormalities in NODAP. The gene discussed is LEP; the disease is pancreatitis.