Given the findings presented in this study, we propose a mechanistic model for targeted inhibition of BRD9 in UFs herein that: (1) BRD9 expression is aberrantly overexpressed in UFs, (2) targeted inhibition of BRD9 reverses the UF phenotype with a decrease in cell proliferation and modulated ECM deposition and remodeling, (3) I-BRD9 modulates several key pathways, and reprograms the pathological epigenome and epitranscriptome, potentially leading to a new strategy for generating effective, precise non-hormonal treatment for UFs (Figure 8C). The gene discussed is BRD9; the disease is Ochoa syndrome.