Part of this may be due to the mechanisms, other than activating mutations in hotspots of NOTCH1 or FBXW7, that activate Notch signaling in T-ALL patients, and which may explain the large overlap in the Notch pathway activity levels for T-ALL patients with and without NOTCH/FBXW7 mutations. This evidence concerns the gene FBXW7 and acute lymphoblastic leukemia.