Checkpoint inhibitors have an anticancer effect by removing a negative regulatory signal for T-cell activation from the tumor microenvironment (Fig. 1). They include cytotoxic T-cell–associated antigen (CTLA-4), programmed cell death protein-1 (PD-1), and programmed cell death ligand-1 (PDL-1) antibodies and are now being widely used for the treatment of different types of cancer. From the initial phases of checkpoint inhibitor use, there has been concern about the potential for the development of autoimmune disease as a result of T-cell activation. Subsequently, multiple autoimmune diseases were indeed observed as a result of these medications (1). Although both PD-1 and PDL-1 antibodies can precipitate type 1 diabetes in the nonobese diabetic mice model (2), only very recent reports have noted type 1 diabetes after PD-1 antibody use in humans (3, 4). Here, we describe two older adults without diabetes receiving agents inhibiting the PD-1 pathway for resistant cancers who developed acute type 1 diabetes. The first patient was a 70-year-old euglycemic male who was started on a PDL-1 antibody for advanced adenocarcinoma of the lung. After 15 weeks and five doses of the medication, he was noted to have plasma glucose of 512 mg/dL, and as he did not have any history of diabetes, he was started on metformin. Ten days later he presented with diabetic ketoacidosis (DKA)(Table 1). He remained insulin dependent and died of his advanced cancer 7 months later.