While we previously observed that cell lines harboring wild-type p53 are more sensitive to 11a compared to those with p53 mutations in the NCI-60 cancer cell panel [21], the hypothesis that 11a’s anti-tumor effects rely on the transcription factor activity of NR2E3 and the following molecular mechanism study conducted with a DR2-reporter and cell lines bearing p53 mutations were not well justified (see supplementary discussion for details). The gene discussed is TP53; the disease is cancer.