TP53 and glioblastoma: Acetylation is essential for basic p53 function, and multiple sites of p53 (including lysines K370, K372, K373, K381, K382, and K386) are acetylated or deacetylated to define the overall level of p53 acetylation.[5] p53 acetylation is crucial for its tumor suppressive functions, and deacetylase inhibitors have shown preclinical efficacy in multiple cancer types, including GBM.[6]