As the NF-kappa B and P53 signaling pathways have been demonstrated to be molecular pathogenesis and therapeutic targets of AML 37, 38 and RhoF can be activated by KLF4, including NF-κB signaling in esophageal keratinocytes 39, it follows that activated RhoF may have the same effect in AML by activating the NF-kappa B. High levels of notch can interfere with the drug response, which can be used as a prognostic marker and therapeutic target in AML 40. The gene discussed is NFKB1; the disease is acute myeloid leukemia.