In addition, we reported that infection with either attenuated (NH/P68) or virulent (22653/14) ASFV impaired the ability of macrophages to secrete pro-inflammatory IL-12, IL-6, and TNF-α in response to stimulation with IFN-γ + LPS or a TLR2 agonist, suggesting that ASFV-infected macrophages were more refractory to external stimuli [21]. The gene discussed is TNF; the disease is infection.