Additionally, as a critical mediator in differentiation and development of myeloid DCs, GM-CSF has been shown to promote DC recruitment in multiple disease applications (41), including the non-obese diabetic (NOD) mouse model of T1D where adoptive transfer of GM-CSF exposed DCs promoted the expansion of Foxp3+ Tregs and delayed diabetes onset (42). This evidence concerns the gene CSF2 and diabetes mellitus.