Mesenchymal stem cells (MSCs) are recognized for their potential in regenerative medicine. Due to long-term negative effects associated with insulin administration and difficulty with pancreas transplantation, patients with type-1 diabetes could significantly benefit from organ-targeted cell-based therapy. Although several pharmacological agents increase the homing capacity of MSCs, the mechanisms regulating this process are still poorly understood. In this issue, Najafi et al. have demonstrated that pre-treatment of bone marrow-derived MSCs with the iron chelator and hypoxia mimetic, deferoxamine, can increase homing to the pancreas in a rat model of diabetes. This effect appears to be driven through specific chemokines in addition to hypoxia-inducing factor 1-alpha. Results from this study provide important clues in our endeavour to solve a complex process. Further studies will help determine whether these findings may offer potential therapeutic benefit to patients with diabetes.