In cells with a high MYC burden, therefore, MYC that is bound at enhancers may be particularly sensitive to inhibition, and the tumor-suppressive functions of SNF5 could act within the context of SWI/SNF to both maintain normal patterns of open chromatin status at key enhancers and to resist cooption of enhancer function by ectopic MYC. The gene discussed is MYC; the disease is neoplasm.