In support of this, priming macrophages with the synthetic TLR1/2 agonist, Pam3CSK4, that exclusively engages MyD88 and not TRIF signalling to induce expression of anti-apoptotic proteins, likewise sensitised macrophages to TRIF-dependent necroptosis following ΔespL infection (Figs. 4F and EV4A). The gene discussed is TLR1; the disease is infection.