A very recent article has demonstrated that a combined treatment consisting of low concentrations of retinoic acid (RA), of the ER stressor tunicamycin, and of arsenic trioxide (ATO), led to ER and oxidative stresses as well as to UPR in AML cells expressing fusion proteins such as MLL-AF4, MLL-AF6, MLL-AF9, or FLT3-internal tandem duplication (ITD), alone or in combination. The gene discussed is KMT2A; the disease is acute myeloid leukemia.