In addition, bortezomib has recently emerged as a potential modulator of the oncogenic T-ALL driver NOTCH1. In fact, preclinical studies showed that bortezomib suppresses the expression of Notch and its target genes (HES1, GATA3, and RUNX3) and synergizes with dexamethasone, leading to a near-complete remission of T-ALL xenografted tumors in vivo,30 supporting the rationale of several ongoing clinical trials (eg, ClinicalTrials.gov identifiers: NCT02518750 and NCT03643276). This evidence concerns the gene RUNX3 and acute lymphoblastic leukemia.