Despite the potential impact on the IFN-γ axis, patients with IRF4 haploinsufficiency appear to be selectively susceptible to WD without susceptibility to other intracellular pathogens that rely on intact IFN-γ/STAT1 signaling (e.g. mycobacteria,Salmonella, etc.), implying that other parallel and/or compensatory immune mechanisms may play a role. This evidence concerns the gene IRF4 and Wilson disease.