Indeed, the inhibition of Notch1 signaling by a GSI Compound E suppressed HES1, restored glucocorticoid receptor (NR3C1) auto-upregulation, and induced apoptotic cell death through BCL-2L11 induction in a model of glucocorticoid-resistant T-ALL [190]. This evidence concerns the gene BCL2L11 and acute lymphoblastic leukemia.