The molecular mechanism underlying targeting NAT10 oncogenesis in AML was explored, and NAT10 inhibition was found to induce apoptosis in association with ER stress induction, triggering the unfolded protein response (UPR) pathway and further activation of the classical apoptosis pathway through BH-3 proteins (Bim and PUMA). Here, BCL2L11 is linked to acute myeloid leukemia.