Both in murine myeloid 32D cells stably transformed with BCR-ABL (32D/BCR-ABL cells) and in K562 cells (a human BCR-ABL+ CML cell line), it was found that BCR-ABL1 kinase activated the PI3K/Akt signaling cascades, and abolished the repression of forkhead box protein O4 (FOXO4) on activating transcription factor 5 (ATF5), leading to activation of mTOR and then inhibition of the autophagic pathway [9]. The gene discussed is BCR; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.