Considering the knockout of the type I IFN receptor (Ifnar1) or TLR7, which is particularly linked to the female-prevalent pathogenesis of PBC and LN in ARE-Del mice [30,31], the increase in type I IFNs induced by IFN-γ may be associated with macrophage dysfunction, likely due to the mitochondrial metabolic imbalances required for proper functioning. The gene discussed is IFNG; the disease is lobular neoplasia.