Latent autoimmune diabetes of adults (LADA) is a subset of type 1 diabetes. The disease accounts for ∼2–12% of all cases of diabetes (1). The pathogenesis of the disease involves autoimmune destruction of the β-cells of the pancreatic islet that produce insulin. There is a cell-mediated effect, via islet-reactive T cells (2), and a humoral immune response via autoantibodies (3). Studies have indicated that the GAD and islet cell antibodies are the most common in patients with LADA (4). Despite the priority of hyperglycemia, treating the underlying pathogenesis should be considered. Some of these efforts may include interfering with the cytokines that are implicated in the inflammatory process, which include tumor necrosis factor-α and interleukin-1β, among others. A tumor necrosis factor-α blocker, …