Notably, more than 50% of human T-ALL patient samples show activating Notch1 mutations9, 52 whereas overexpression of Notch3, irrespective of gross abnormalities in the Notch3 locus, is a common finding in human T-ALL,8 raising the possibility that in this context high Pin1 expression might contribute to sustain high levels and function of N3IC protein, similarly to what happens for Notch1 in breast cancer where it is rarely mutated.20, 53 Mechanistically, we show that Pin1 interacts directly with phosphorylated Notch3 and increases N3IC protein expression. The gene discussed is NOTCH3; the disease is acute lymphoblastic leukemia.