Although TNLs have been characterized principally as pathogen effector-sensing devices with direct ETI roles in cells that are destined to die, a suite of TNL and TIR-domain genes are upregulated in cell-surface receptor mediated PTI [34,134], consistent with TNL and TIR enzymatic activities (§4) also stimulating immune responses in non-dying cells bordering infection sites. Here, TRIM67 is linked to infection.