This is consistent with previous reports showing that ATG4B exhibits overlapping redundancies in autophagy in some cancer cells.[42, 43] In this study, we provide evidence demonstrating a novel role of ATG4B, beyond its involvement in autophagy, in the progression of AML by reducing PRMT1, which plays a critical role in DNA damage repair. This evidence concerns the gene PRMT1 and acute myeloid leukemia.