Given the overwhelming evidence that allo- and auto-immune responses against ACE-transplanted islets mirror those in the pancreas and other transplant sites (92, 134–140), the current findings suggest that our SMIPPIs likely inhibited the activation and priming of T effector cells, which in turn reduced their infiltration into the islet allografts and consequently promoted the long-term survival and function of the islets in both transplant sites (i.e., kidney and ACE) and, possibly, the native pancreas of the NOD mice that never progressed to diabetes (Figure 7). The gene discussed is ACE; the disease is diabetes mellitus.