In addition, our results demonstrated that the increase in cellular drug resistance mediated by high NR6A1 expression was mainly achieved by upregulating the S100A4 expression level, in other words, even though NR6A1 expression was elevated when the S100A4 expression level was knocked down, it did not increase the resistance of AML cells to cytarabine. The gene discussed is NR6A1; the disease is acute myeloid leukemia.