However, the development of temporal, mild hyperglycemia post-therapy associated with suppression of in situ islet PDX-1, insulin and PP, both known to regulate glucose homeostasis [15], [16], [17] and increased islet apoptosis, demonstrate that systemic delivery of bi-shRNAmousePDX-1 lipoplexes are reaching their PDX-1 target. The gene discussed is PPY; the disease is Hyperglycemia.