We found that in p53-mutant cells and p53-WT cells overexpressing a p53 mutant, which were only modestly affected by HDAC1 silencing, p-STAT3 levels were already elevated at baseline and did not change after HDAC1 loss — this is in line with previous studies that have shown cancer cell lines that harbor p53 mutations or deletions express constitutively active STAT3 (Figure 7C, Supplemental Figure 7, and refs. 56, 92, 93). The gene discussed is STAT3; the disease is cancer.