Tau protein methylation can be protective because, while multiple sites of tau are heavily acetylated in the AD brain, these sites are preferentially methylated [90]; enzymes involved in this protective function, such as PP2A, can be regulated by methylation, and the inhibition of PP2A leads to increased and aberrant levels of phosphorylation in combination with reduced intracellular methylation, resulting in the hyperphosphorylation of tau protein. This evidence concerns the gene PTPA and Alzheimer disease.