Both compound 16, a small molecule WDR5 WIN site inhibitor, and WDR5 knockdown have been shown to reduce expression of genes involved in H3 K4 trimethylation and associated oncogenic pathways, thereby inhibiting GSCs growth and self-renewal in vitro, as well as tumor growth in a flank GBM xenograft model [231, 232]. Here, FOXM1 is linked to glioblastoma.