Finally, as we observed in HG-CD34+-derived monocytes, the epigenetic analysis of NFkB-p65 promoter in CAD-T2DM-derived monocytes revealed pro-transcriptional H3K4me1 mark accumulation that, following our hypothesis, was the faithful reflex of the “fixed” HSPC reprogramming promoted by T2DM in the BM. The gene discussed is CD34; the disease is coronary artery disorder.