AKT1 and chronic myelogenous leukemia, BCR-ABL1 positive: In conclusion, our studies identify a novel miR-155-dependent mechanism of regulating the aberrant oncogenic activity of the Stat5 and PI3K/AKT/mTOR signaling in the persistent IM-resistant the Bcr-Abl+CD34+/CD38− hCSCs, which are major culprits in the altered growth, drug resistance, and recurrence observed in CML patients (Figure 5).