Interestingly, these distinct differences of altered gene expression pathways between ‘high-repeat’ and ‘low-repeat’ AML patient subgroups were in addition to upregulated Toll-like receptor signaling, NFκB activation and interferon signaling, which appeared to be similarly stimulated in both ‘high-repeat’ and ‘low-repeat’ AML patient subgroups compared to the CD34+ (blueprint) control cells [22]. Here, NFKB1 is linked to acute myeloid leukemia.