TBP and malignant endocrine neoplasm: Targeting ID proteins by small molecules to block protein‐protein interactions is a rapidly evolving field, and our findings suggest that compounds that could block AF1‐TBP interaction sites may provide potential avenues to modify AF1 activity needed for additional selectivity to target cell‐tissue specific gene regulations of SHRs, which could complement or replace existing SRMs actions in current SHR‐based endocrine cancer therapies.