In vivo studies have reported that APP is a substrate for ROCK1, and activationof ROCK1 enhances APP cleavage by β-secretase, increasing Aβlevels and promoting the pathogenesis of AD. Furthermore, inhibition of APP phosphorylation or inhibition ofROCK activity through knockdown or using an inhibitor improved learningand memory in APP/PS1 mice. Another studyshowed that the selective inhibition of ROCK2 suppressed the enzymaticactivity of the BACE1 enzyme, decreasing Aβ productionin vivo. This evidence concerns the gene APP and Alzheimer disease.