Considering these data, we propose a revised model for thinking about how rSWI/SNF complexes maintain aberrant transcriptional programs in rhabdoid tumors: SNF5 normally functions to both temper MYC binding to chromatin [7, 19] and activate enhancers controlling differentiation and development genes [3, 4], the combination of which allows for the integration of signals dictating normal cell growth during development. Here, SMARCB1 is linked to rhabdoid tumor.