MYD88 and pancreatic neoplasm: LPS was shown to drive pancreatic carcinogenesis, as was the blockade of the MyD88-dependent pathway (via a dendritic cell-mediated deviation to TH2), whereas blockade of TLR4 (via TRIF, TIR-domain-containing adapter-inducing interferon-β) and blockade of the MyD88 independent (via TRIF) were protective against pancreatic cancer (63).