For example, focusing only at MxA, a protein classically characterized as type I IFN-specific, would have led to the conclusion that both atopic dermatitis datasets showed an average of 2.9-fold overexpression relatively to healthy controls (data not shown); this could be misconstrued as evidence of type I IFN activation in the skin of atopic dermatitis, which is clearly not the case. This evidence concerns the gene MX1 and atopic eczema.