The first answer appears straight-forward: In PD, inhibition of SIRT2 reduces α-synuclein aggregation and toxicity by modifying the levels of acetylation of this protein [5]; in AD, SIRT2 is abnormally overexpressed and deacetylates tubulin which results in microtubule destabilization, Tau dissociation from microtubules, and subsequent oligomerization and aggregate formation [6]. The gene discussed is SIRT2; the disease is Parkinson disease.