These findings are consistent with the reported differential immunomodulatory effects between selective and pan-HDAC inhibitors.20 Toll-like receptors (TLRs) are known to initiate acute inflammatory responses and chemokine production, and further activate antitumor immune responses in vivo.41 Importantly, TLR3 activation induces tumor cells to produce type I interferons, which are indispensable for T cell-mediated antitumor immune responses.40 We observed a significant increase in TLR3 expression after PM treatment. The gene discussed is TLR3; the disease is neoplasm.