In our work, we discovered that the AT subtype is significantly more resistant to BET inhibition than other HNSCC subtypes, and that this resistance seems, at least in part, mediated by increased enhancer activity on pathways associated with lipid and cholesterol metabolism, MAPK signaling, and WNT-β-​catenin signaling. The gene discussed is DNER; the disease is head and neck squamous cell carcinoma.