Pancreatic beta-cells play a pivotal role to synthesize and secrete insulin, as the solo source of the body. Physical as well as functional loss of beta-cells over a certain threshold result in diabetes. While the mechanisms underlying beta-cell loss in various types of diabetes have been extensively studied, less is known about residual beta-cells, found even in autoimmune type 1 diabetes and type 2 diabetes with a substantial amount. Why have these beta-cells been spared? Some patients with neonatal diabetes have demonstrated the life-changing restoration of functional beta-cells that were inactive for decades but awakened in several weeks following specific treatment. The recent striking outcomes of bariatric surgery in many obese diabetic patients indicate that their beta-cells are likely “preserved” rather than irreversibly lost even in the multifactorial polygenic state that is type 2 diabetes. Collectively, the preservation of residual beta-cells in various diabetic conditions challenges us regarding our understanding of beta-cell death and survival, where their sustenance may stem from the existence of resting beta-cells under physiological conditions. We posit that beta-cells rest and that studies of this normal feature of beta-cells could lead to new approaches for potentially reactivating and preserving beta-cell mass in order to treat diabetes.