Further, in a cancer cell line defined by deficiency in both SMARCA4 and SMARCA2 expression and hence lacking the entire ATPase module (BIN-67 SCCOHT cells60–63, we found that expression of PU.1 or GATA3 resulted in substantial redirection of core module occupancy on chromatin (Fig. 2H, S4B–E), with TF-specific de novo mSWI/SNF sites showing corresponding motif enrichment (Fig. 2I). This evidence concerns the gene SMARCA2 and cancer.