Signaling through PI3K/AKT inhibits autophagy in BCR-ABL–transformed cells. (A) Immunoblot analysis monitoring the levels of phosphorylated AKT, ATF5, LC3B, and ACTB in 32D/BCR-ABL cells treated in the absence or presence of LY294002 (20μM for 48 hours). (B) Immunoblot analysis monitoring the levels of phosphorylated AKT, ATF5, LC3B, and ACTB in 32D/BCR-ABL cells expressing either empty vector or a vector encoding PIK3CA(E545K). (C) Immunoblot analysis monitoring phosphorylated AKT, ATF5, and LC3B levels in 32D/BCR-ABL cells treated with imatinib (5μM for 24 hours). (D) Immunoblot analysis monitoring phosphorylated AKT, ATF5, and LC3B levels in imatinib-treated 32D/BCR-ABL cells (5μM for 24 hours) expressing empty vector or PIK3CA(E545K).