Consistent with previous studies showed that hyper-activation of FAT10 increased the potential of tumorigenesis [20, 48, 49], we demonstrated that loss of Celf2 increased MA9-induced AML initiation by upregulating FAT10 expression, thus increasing AKT phosphorylation, and subsequent activation of mTORC1 (Fig. 5). The gene discussed is UBD; the disease is acute myeloid leukemia.