Interestingly, preliminary results of proteomic studies following knock‐down of filaggrin in epidermal equivalents (to mimic the effects of filaggrin deficiency in atopic eczema skin) identified a number of differentially expressed proteins that included cyclophilin A, further underscoring a potential role for cyclophilins in atopic eczema pathogenesis.30 Moreover, our early studies of methotrexate in skin equivalents showed a positive effect on late terminal differentiation in keratinocytes, emphasizing the relevance of the epidermal barrier as a therapeutic target.31 This evidence concerns the gene PPIB and atopic eczema.