In particular, in murine models of Notch3- and Notch1-dependent T-ALL, Notch signaling sustained the canonical p50/p65 NF-κB pathway by interacting with the IKK (Inhibitor of NF-κB (IκB) Kinase) signalosome, and consistently, independent studies demonstrated that combined pharmacological inhibition of Notch and NF-κB strongly enhanced cell growth arrest and apoptosis in T-ALL [109,110,111,112,113]. The gene discussed is NOTCH1; the disease is acute lymphoblastic leukemia.