found that the CD56 expression on AML cells correlates with an abnormal expression pattern of runt-related transcription factor 1 (RUNX1) isoforms and the potential for new therapy of CD56(high) AML by suppression of the “overactive” RUNX1/CD56/NF-kappa B signaling pathway(s) (22). Here, NCAM1 is linked to acute myeloid leukemia.