CDKN1A and neoplasm: Reactivated p73 is free to promote the expression of anti-tumorigenic genes, including CDKN1A (p21) and BBC3 (PUMA), resulting in cell-cycle arrest and apoptosis.14 Notably, we showed that tamoxifen increased ERβ-mutant p53 interaction, and p73-mutant p53 interaction was reciprocally decreased leading to the reactivation of p73 as a tumor suppressor.