Simultaneously, it was also indicated that drug resistance in T-ALL patients could be mediated by the interaction and deubiquitination between USP1 and Aurora B. Mechanistically, further studies confirmed that ALKBH5 enhanced USP1 expression via modulating USP1 RNA m6A demethylation levels and elevating mRNA stability; downregulation of ALKBH5 could decrease USP1 and Aurora B levels to promote the sensitivity of CEM-C1 cells to Dex and inhibited the proliferation of tumor cells. The gene discussed is USP1; the disease is neoplasm.