**4. Conclusions**

The robust evidence pointing towards involvement of RAGE and its ligands in inflammation and autoimmunity paves a new pathway towards understanding the pathophysiology of T1DM. Valuable lessons can also be learned about approaches to undertake when designing new therapies to target this axis from previous findings. Further understanding of the role of greater RAGE expression on immune cells and pancreatic islets during T1DM pathogenesis is required and is likely to be multifaceted given the myriad of inflammatory diseases which involve RAGE mediated processes. T1DM is incredibly complex and heterogeneous disorder, and it is unlikely for a 'silver bullet' therapy to emerge. This highlights the importance of exploring alternative mechanistic pathways for therapy which have not been previously considered. Indeed, it is likely that the best approach to T1DM may be combination therapies which are targeted towards various aspects of disease and provide greater coverage of the vast immune dysfunction which may be present.
