Maier, et al. [29] reported that eIF5A depletion as well as the inhibition of hypusination protected against glucose intolerance in inflammatory mouse models of diabetes and that knockdown of eIF5A made mice resistant to β-cell loss and the development of hyperglycemia in the low-dose streptozotocin model of diabetes. The gene discussed is EIF5A; the disease is Glucose intolerance.