SP1 and cancer: Notably, multiple reports have shown that p300 interacts with Sp1 or β‐catenin in various cancers, contributing to the acquisition of a malignant phenotype and drug resistance.[31, 32] Subsequently, we conducted a ChIP assay, revealing that NR2E3 depletion increased not only p300 recruitment but also active histone marks, in particular histone three lysine 27 acetylation (H3K27Ac), a substrate of p300, within these promoter regions (Figure 6K).