Finally, normalizing the expression of only the HMGN1 gene in the Ts1Rhr mouse DS model rescued B cell pathological phenotypes, abolished an increase in H3K27ac marks, and mitigated mRNA expression changes, indicating that the increased dosage of HMGN1 is sufficient to induce DS-specific transcriptomic and epigenetic signatures and cellular phenotypes in B cells. This evidence concerns the gene HMGN1 and Dravet syndrome.