Based on these data, we propose a mechanistic model in which: (1) BRD2 and BRD4 are aberrantly upregulated in UFs, (2) BET inhibition suppresses UF phenotypes by reducing proliferation, inflammation, transcriptional activity, and ECM expression, (3) JQ1/I-BET762 treatment reprograms the pathological epigenome and modulates key signaling pathways, leading to inhibition of UF growth (Figure 11). Here, BRD4 is linked to Ochoa syndrome.