One possible explanation for this divergent influence on different EPCs populations is that pre-diabetes reduces EPCs survival (with subsequent reduction CD45dimCD34+KDR+ EPCs levels) but, does not impair neither bone marrow recruitment of EPCs (leading to no differences in levels of CD45dimCD133+KDR+ EPCs) nor homing processes (explaining the normal proportion of EPCs coexpressing CXCR4). The gene discussed is KDR; the disease is diabetes mellitus.