This included (i) decreased viability and downregulation of Wnt/β-catenin signaling after BAZ2A genetic knockout (Fig. S4A–E), (ii) modest effects of the BAZ2-specific bromodomain inhibitor BAZ2-ICR [52] (Fig. S4F–I), and (iii) significantly reduced tumor growth for BAZ2A knockout cells in nude mice (Fig. S5A), with a concomitant reduction in Wnt/β-catenin signaling and histone protein expression in tumor xenografts (Fig. S5B and S5C). Here, ZNF215 is linked to neoplasm.