Background: Background:Gain-of-function NOTCH1 mutations are the most common genetic abnormality in T-cell Acute Lymphoblastic Leukemia (T-ALL), accounting for 55-60% of the cases. Consequently, modulators of the Notch pathway, such as γsecretase inhibitors (GSI), would be expected to have clinical efficacy (Rao, Cancer Res 2009). However, their application was limited by an excess of toxicity due to the suppression of wild-type (WT) NOTCH1 proteins in normal tissue (Deangelo, JCO 2006; Doody, Alzherimer's Res Ther 2015).
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