It has been demonstrated that several fusion oncogenes, notably PML-RARα in Acute Promyelocytic Leukemia (APL) [82], BCR-ABL in Chronic Myelogenous Leukemia (CML) [83], and FLT3-ITD in Acute Myeloid Leukemia (AML) [84] can be degraded through autophagy induced by specific treatment, i.e., arsenic trioxide or all-trans retinoic acid in APL; arsenic trioxide in CML and an inhibitor of the proteasome known to induce autophagy, the bortezomib, in AML. The gene discussed is PML; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.