As synaptic plasticity is a leading candidate mechanism for information and memory storage, and due to the fact that we identified regulation of ion channels and receptors as a candidate mechanism for Hp1bp3‐induced cognitive impairment in an aging mouse population (Neuner et al., 2016), we were particularly interested in the most significantly downregulated GO term, regulation of neuronal synaptic plasticity. This evidence concerns the gene HP1BP3 and Cognitive impairment.