This differential outcome is one of the reasons we selected MPL as the TLR agonist for our in vivo studies (Fig. 7), because even though MPL signals through TLR4, it has been suggested to bias towards TRIF-mediated, as opposed to MyD88-mediated signalling and so may have some of the benefits of TRIF-dependent tumour suppression26. Here, MYD88 is linked to neoplasm.