Because retained SWI/SNF complexes promote aberrant genomic activities in SWI/SNF-altered cancers—some of which occurs through interactions with MYC on chromatin [19]—we also analyzed chromatin immunoprecipitation sequencing (ChIP-seq) data that are publicly available for the SWI/SNF subunit BAF155 in BIN-67 cells [15]. This evidence concerns the gene SMARCC1 and cancer.