These results suggest that LXR-induced STAT5 and NF-κB inhibitions may be involved in both the inhibition of cell proliferation and BPDCN cell death, demonstrating a new therapeutic approach where cholesterol homeostasis is modified in BPDCN and normalized by treatment with LXR agonists. Here, NFKB1 is linked to CD4+/CD56+ hematodermic neoplasm.