Notably, the absence of ER or AHR has been associated with the enhanced development of HCC in murine models.[39, 40] NR2E3 loss resulted in p53 inactivation through epigenetic DINO repression in an acetaminophen‐induced hepatotoxicity model.[8] These findings strongly indicate that NR2E3 functions as a tumor suppressor and an epigenetic regulator in the context of HCC. Here, TP53 is linked to neoplasm.