Crossing eNOS knockout (eNOS−/−) mice with a mouse model of amyloid pathology (APP/PS1 mice) was associated with increased phosphorylated tau (p-tau), which was attributed to an increase in Cdk5 activation by p25, while other kinases, such as GSK-3β, were unchanged [176,177]. This evidence concerns the gene NOS3 and amyloidosis.