Conventionally, type 1 diabetes (T1D) is defined as a disease caused by autoimmune destruction of the β cells of the pancreas leading to insulinopenia and consequent persistent hyperglycemia. The diagnosis of T1D and the introduction of insulin therapy may be followed by a period of partial β-cell recovery and the production of endogenous insulin. This phase of the disease is called the honeymoon phase or partial clinical remission (PR) phase. PR is a crucial period where interventions can be introduced to modify the clinical course of T1D. Studies have shown that prolonging the PR reduces the short- and long-term complications of T1D. Newer strategies to prolong the PR increasingly show that the classic Eisenbath model of the pathogenesis of T1D, based on β-cell destruction, should be integrated with a newer paradigm of loss of the β-cell function model to explain the heterogeneity of the various endotypes that characterize T1D. This comprehensive approach to T1D pathogenesis allows for pharmacological and non-pharmacological interventions to prolong PR that include strategies to preserve both β-cell mass and function. In this chapter, we present some of the important interventions to prolong the PR phase of T1D, the central role of vitamin D in these interventions, and recommendations for future research.