Althought activating mutations in FLT3 and c-Kit (receptor tyrosine kinase (RTK)), which encode receptor tyrosine kinases upstream of Ras, were shown to be responsible for aberrant activation of Ras signaling in 40% of AML cases [59], Birken and collaborators demonstrated that NF-κB activation in AML blasts was not dependent on FLT3 mutations, but was triggered by RAS and PI3K/AKT (protein kinase B (PKA)) pathways, as the pharmacological inhibition of these two signaling blocked NF-κB activity [60]. The gene discussed is AKT1; the disease is acute myeloid leukemia.