Our ability to physically separate the canonical functions of SNF5 from its anti-MYC activities reveals that SNF5 does not modulate MYC binding via changes in chromatin accessibility, and supports a revised model in which dual regulation of both chromatin accessibility (at TSS-distal enhancers) and control of MYC (at TSS-proximal promoters) are part of the SNF5 tumor-suppression program (Fig. 5). Here, SMARCB1 is linked to neoplasm.