Here, we used MOBSCs from the APP/PS1 mouse model of Aβ pathology, alongside wildtype littermates, to model first, whether we see changes to p-tau Ser356 expression in this AD model, and then the implications of targeting NUAK activity, using WZ4003, under physiological (wildtype) or Aβ pathology (APP/PS1) conditions. The gene discussed is APP; the disease is Alzheimer disease.