Crucially, this observation was also true in the tumor-initiating population, as treatment of AR cells with the PRMT5 inhibitor GSK591 (Duncan et al., 2015) substantially reduced FOXP1 promoter H3K4me3 levels (Figure 6I), and treatment of primary mammospheres with the WDR5 antagonist OICR-9429 (Grebien et al., 2015) reduced BCSC proliferation in a dose-dependent manner (Figure S7G). This evidence concerns the gene FOXP1 and neoplasm.