FOXP1 and breast cancer: Symmetric dimethylation of H2AR3, H4R3 (43), and H3R8 (44) by PRMT5 is linked to transcriptional repression, whereas SDMA at H3R2 (H3R2me2S) supports H3K4me3 (45) and activates FOXP1, which promotes breast cancer stem cell proliferation (46).