Recent findings underscore the pivotal role of tau pathology in the pathogenesis of dementia and suggest that modulating excessive reactive oxygen species (ROS) production, driven by Aβ‐induced NADPH oxidase (Nox) activation, may be crucial in mitigating the progression of tauopathy.[10] Therefore, effectively regulating ROS production through Nox inhibitor can positively influence physiological processes in the brain tissue. This evidence concerns the gene FMO5 and dementia.