In KIT-driven AML, KIT upregulates Sp1, which in turn binds NF-κB and transactivates KIT. Sp1 escapes from miR-29b downregulation through a negative feedback loop, in which Sp1-induced NF-κB recruits HDACs in the miR-29b promoter leading to its transcriptional repression [162]. Here, KIT is linked to acute myeloid leukemia.