Confirming this idea, we found that the knockdown of VAV1 also leads to the upregulation of ICN1 levels in both CEM (carrying heterozygous mutations in Fbxw7 [R465H] and the Notch1 heterodimerization domain [HD]) and Molt4 (bearing heterozygous mutations targeting both the HD and the proline-glutamic-serine-threonine [PEST] motif of Notch1) T-ALL cells (Figures 4I and S4A). This evidence concerns the gene VAV1 and acute lymphoblastic leukemia.