KMT2A and breast cancer: The mechanism by which PRMT5 regulates breast cancer stem cell function involves up‐regulation of FOXP1. PRMT5 binds to the FOXP1 promoter and induces symmetrical methylation of histone H3R2, which in turn promotes recruitment of the WDR5 subunit of the SET1/MLL methyltransferase complex that is known to methylate H3K4me3, resulting in elevated expression of FOXP1. These results indicate that PRMT5 plays an important role in maintaining breast cancer stemness.26