In agreement with the in vivo data, bone marrow-derived macrophages (BMDMs) from Trim56-deficient mice are defective for IFN-α/β production following HSV-1 mutant γ34.5 virus (mutHSV-1) infection, in contrast to WT BMDMs that allow for significant type I IFN induction [34]. The gene discussed is IFNA1; the disease is infection.