Hence, we sought to determine whether (1) selective NOTCH1 inhibition could reduce LIC burden, (2) NOTCH1Mutated T-ALL LIC survival is dependent on activated NOTCH1 receptor signaling, and (3) selective NOTCH1 inhibition could spare NOTCH1WT or normal cord blood CD34+ progenitors in engrafted mice. This evidence concerns the gene NOTCH1 and acute lymphoblastic leukemia.