In the case of Kabuki syndrome 1, which is predicted to have loss of the transcriptionally activating mark H3K4me3 at promoters, the Björnsson group showed that either inhibition of the opposing H3K4 demethylase (63) or HDAC inhibition through pharmacological or diet-induced means was also sufficient to improve hippocampal function and visual-spatial learning in mice (61, 62). This evidence concerns the gene HDAC9 and Kabuki syndrome 1.