Cao et al. [23] found that administration of the SET1/MLL inhibitor WRD5-0103 inhibited the increase in H3K4me3 levels and the down-regulation of glutamatergic synaptic receptor expression, and restored synaptic plasticity in the prefrontal cortex, thus alleviating cognitive deficits in P301S Tau mice and five familial AD mutations mice. The gene discussed is KMT2A; the disease is Alzheimer disease.