In addition, reports have found that JUN is activated by MEK signaling in response to endoplasmic reticulum stress, and JUN binds to the promoters of several key UPR effectors (such as XBP1 and ATF4) to activate their transcription and allow AML cells to correctly regulate endoplasmic reticulum stress [46]. This evidence concerns the gene XBP1 and acute myeloid leukemia.