The FOXO1 TF, a major downstream effector of the PI3K/AKT pathway, is negatively regulated through AKT-mediated phosphorylation and inactivation of FOXO1 has been implicated in the development of pre-B ALL.22–24 Following the treatment of CUDC-907, the decrease in AKT expression and phosphorylation resulting in an upregulation of FOXO1 expression and reactivation of its target genes related to pre-B cell development program (Supplementary Fig. 3a, b). This evidence concerns the gene PIK3CB and acute lymphoblastic leukemia.