As a clinical counterpart, bone pain, which is caused by G-CSF acting on the BM and correlates with the extent of mobilization, is alleviated by diabetes and is associated with an impaired HSPC release.38 Therapeutically, mobilopathy due to BM neuropathy could be overcome by deleting the redox enzyme p66Shc that drives oxidative stress nerve damage, by overexpressing the longevity protein Sirt-1, by boosting the residual nerve function with the norepinephrine reuptake inhibitor desipramine,39 or by stimulating nerve regeneration with nerve growth factor.41 Here, CSF3 is linked to diabetes mellitus.