These distinct differences of altered gene expression pathways between ‘high-repeat’ and ‘low-repeat’ AML patient samples are in addition to upregulated Toll-like receptor signaling, NF-kb activation and interferon signaling, which are similarly stimulated in both ‘high-repeat’ and ‘low-repeat’ AML patient subgroups as compared to the CD34 + (Blueprint) control cells (see Additional file 9: Figure S9). Here, NFKB1 is linked to acute myeloid leukemia.