Nonetheless, a number of recent preclinical investigations demonstrate that the leukemic transcription program is activated by NPM1c chromatin-binding to target gene promoters and highly dependent on wild-type KMT2A-menin interaction as either genomic editing or pharmacological inhibition of menin suppress pro-leukemic gene expression and lead to hematopoietic differentiation in NPM1c AML models (Klossowski et al., 2019; Kühn et al., 2016; Uckelmann et al., 2020, 2022; Wang et al., 2022). The gene discussed is MEN1; the disease is acute myeloid leukemia.