Subsequent investigations led to the identification of a slightly different mechanism of NRF2 inhibition in acute myeloid leukemia (AML) and acute promyelocytic leukemia (APL) cells, wherein ATRA was shown to prevent the nuclear accumulation of NRF2 in response to arsenic trioxide (ATO), enhancing its cytotoxicity due to impaired transactivation of antioxidant target genes [348] (see Table 2). Here, NFE2L2 is linked to acute myeloid leukemia.