BCR-ABL1-dependent activation of PI3K/AKT signaling contributes to CML LSCs maintenance, as it leads to AKT-mediated phosphorylation and cytosolic retention of FOXO, hence blocks the transcription of FOXO target genes involved in apoptosis [63]. This evidence concerns the gene AKT1 and chronic myelogenous leukemia, BCR-ABL1 positive.