NR4A1/NR4A3 silencing in AML is mediated through the blockade of transcription elongation, while treatment with dihydroergotamine (DHE) rescued NR4A silencing and allowed their tumor-suppressing ability to reactivate with concomitant slowing of AML progression in vivo (Boudreaux et al., 2019). Here, NR4A3 is linked to neoplasm.