Recent studies demonstrated that targeting the interaction between WDR5 and MLL1 via the WDR5-specific inhibitor WDR5-47 can effectively antagonize MLL1 activity of catalyzing H3K4me3 enrichment, resulting in the downregulation of target genes such as PD-L1 and OPN to activate CTLs’ function and suppress pancreatic tumor growth [18,19]. Here, KMT2A is linked to pancreatic neoplasm.