The HDAC inhibitor sodium valproate/valproic acid (VPA) partially restored MHC-II expression and circumvented the enhanced tumor growth in DcR3-transgenic mice inoculated subcutaneously with murine colon adenocarcinoma cells, indicating that epigenetic modulation of TAM differentiation and MHC-II expression had a crucial role in DcR3-driven tumor progression [56, 57]. This evidence concerns the gene HDAC9 and neoplasm.