The inverse connection between CMA and AD pathological markers has been indicated, where mutant variants of Tau that drive Tau hyperphosphorylation (Iqbal et al. 2010) have been found to bind to LAMP2A to impair CMA activity (Wang and Lu 2022), which in turn fosters further accumulation of p-Tau in a self-perpetuating cycle (Wang et al. 2009). This evidence concerns the gene MAPT and Alzheimer disease.