In addition, since Notch1 on/off states combined with changes in NOTCH3 expression levels in Notch1-dependent T-ALL cell lines MOLT3 and P12 and given that Notch3 activity strictly correlated with NOTCH1 expression in Notch3-dependent TALL-1 cells, we hypothesized that the reciprocal regulation by which Notch receptors modulate each other's transcriptional activity could represent a mechanism by which either Notch self-sustains a positive-feedback loop in T-ALL. The gene discussed is NOTCH1; the disease is acute lymphoblastic leukemia.