AP4B1 and Cognitive impairment: This finding has also been described in a previously published murine model of AP-4 deficiency syndrome in which the epsilon subunit of AP-4 was disrupted, suggesting it is a phenotype consistent in mice lacking functional AP-4.13 As the Ap4b1 (−/−) mice in this study clearly have reduced motor function—demonstrated by their performance on the rotarod apparatus—we hypothesise that the increased ambulation is related to an undetermined cognitive defect in the mice.