A major defect in the pathogenesis of type 2 diabetes is the loss of pancreatic β-cell function. This manifests mainly as a reduction in glucose-stimulated insulin secretion. In β-cells, insulin is packaged and stored in insulin secretory granules. Upon stimulation, these granules mobilize and fuse with the plasma membrane, delivering insulin to the bloodstream. The insulin secretory pathway has two critical components: granule biogenesis and granule release. Current anti-diabetic drugs that target the β-cell focus solely on increasing granule release and have no direct effect on the granule biogenesis pathway. This approach is only effective for a short period and cannot prevent the continued decline in β-cell function and glycaemic control. We believe that the key to improving and more importantly maintaining β-cell function in type 2 diabetes relies more on the quality of those secreted granules and less on increasing the number of granules released. The availability of high-quality granules is dependent on optimal regulation of the granule biogenesis pathway. In this talk, I will describe some of the significant advances our team has made in our understanding of the critical but surprisingly poorly understood processes of insulin secretory granule biology.