Several epithelial and hematological malignancies show constitutive NF-κB activation, which could lead to reduction in NSD1 levels.21 Although NSD1 has been described as an oncogene in leukemia, this oncogenic function is only in the context of NUP98–NSD1 fusion gene where the fusion protein increases H3K36me3 specifically at the HoxA locus and increases HoxA expression.12 NF-κB inhibition in this context is less likely to cause upregulation of NUP98–NSD1, because NUP98 regulatory region drives this fusion gene expression. This evidence concerns the gene NSD1 and leukemia.