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. Here, NFKB1 is linked to coronary artery disorder.