Selective overexpression of ERβ in p53-mutated GBM cells failed to restore TSN cytotoxicity (Figure 4D,E), whereas silencing wild-type p53 abrogated TSN-induced GBM cell apoptosis (Figure 5A,B), all of which strongly support a causal association between ERβ upregulation and p53 activity in response to TSN treatment. Here, ESR2 is linked to glioblastoma.