SIRT1 and posterior cortical atrophy: More recently, Baptista, et al. using PCa cell lines showed that H2A.Z regulates its own expression by increasing its accumulation nearby the TSS of the H2AFZ gene, while its regulation is impaired by decreased expression and protein levels of the histone deacetylase NAD-dependent protein deacetylase sirtuin-1 (SIRT1), which is necessary to maintain H2A.Z levels [101].