We found that Nrf2 was highly expressed in AML patients with relapsed and refractory and genetic mutations, and Nrf2 overexpression might inhibit RFC4 by interacting with the RFC4 promoter region binding site and activating the p65/c-Jun/JNK pathway, thereby increasing the resistance of acute myeloid leukemia to cytarabine. Here, JUN is linked to acute myeloid leukemia.