Mechanistically, the SIRT2 and p73 proteins were co-localized in the nucleus in glioblastoma patient samples, suggesting that the SIRT2-mediated deacetylation of p73 is a major cause of the inhibition of p73 transcriptional activity that allows glioblastoma cells to escape p73-mediated proliferation arrest and apoptosis [115]. Here, TP73 is linked to glioblastoma.