Although posttranslational Tau protein modifications may be mediated by many factors, mitochondrial autophagy (also known as mitophagy), reactive oxygen species (ROS), the activation of the NOD-like receptor protein 3 (NLRP3) inflammasome, and the regulation of kinases and phosphatases have attracted attention due to their upstream and downstream effects on tauopathy [10–12]. This evidence concerns the gene NLRP3 and tauopathy.