For instance, in TNBC, the synthetic peptides targeting EN1 protein‐protein interaction domains have been shown to induced cellular apoptotic responses in vitro.[18] Likewise, targeting strategies of other interacting proteins in TNBC, such as TLE3, TRIM24‐TRIM28‐TRIM33 complex[23] and BRD4‐S,[53] might attenuate EN1‐mediated aggressive cancer phenotypes in the breast cancer context. This evidence concerns the gene TRIM24 and cancer.