Indeed, increased dosage of the high mobility group nucleosome-binding protein N1 (HMGN1) has been shown to upregulate B-cell-specific transcriptional signatures in DS-ALL as well as subtypes of B-ALL harbouring gain of chromosome 21, by antagonising the PRC2 complex (reduced H3K27me3 marks) and increasing chromatin accessibility (increased H3K27ac marks) [159]; notably, HMGN1 has also been shown to cooperate with the transcript fusion AML1-ETO9a to promote AML [188]. Here, HMGN1 is linked to acute myeloid leukemia.