In addition, this research group also found that EGFR-activated PKM2 phosphorylated H3-Thr11 can recruit immune checkpoint-related molecule programmed cell death 1 ligand 1 (PD-L1) promoter region to enhance PD-L1 transcription, thereby possibly promoting the formation of immune suppressive tumor microenvironment in HCC.[30] These studies indicate that nuclear PKM2 can promote the expression of genes such as DKK1 and PD-L1 by phosphorylating histone H3, thereby promoting liver cancer cell proliferation, migration, and invasion as well as immune escape. Here, PKM is linked to neoplasm.