On the other hand, silencing of DUSP1 in HCC and oral cancer activates p38, ERK1/2, and JNK pathways that can modulate polarization of TAMs toward the M2 (anti-inflammatory) phenotype,153,154 and isoforms DUSP1, DUSP4, DUSP5, and DUSP6 potentially modulate TAM maturation and polarization.152. This evidence concerns the gene DUSP1 and hepatocellular carcinoma.