Given the role of AP-1 in widespread enhancer malfunction identified in this study, ongoing work will seek to determine if similar alterations in enhancer architecture are also observed in leiomyomas of non-MED12 mutant origins, with AP-1 providing a possible unifying mechanism of gene dysregulation in uterine leiomyomas of differing subtypes. The gene discussed is FOS; the disease is leiomyoma.