Furthermore, we show here that expression of follistatin is strongly down‐regulated in the epidermis of K5‐R1/R2 and K5‐R1/R2/R3 vs control mice, which is likely to result in higher levels of bioactive activin, a potent pro‐fibrotic factor.31, 32 Therefore, the epidermal abnormalities seen in our FGFR mutant mice and also in patients with atopic dermatitis are likely to contribute to the development of skin fibrosis. The gene discussed is FST; the disease is atopic eczema.