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Funding sources: This study was supported by grants from INSERM, Agence National de la Recherche (ANR‐12‐BSV1‐0020‐01) and the Imagine Foundation. R.L. and A.E.B. have received research support from the ERC (ERC PIDImmun 249816) and the ANR, respectively.

Conflicts of interest: none declared.

S.L.M., R.L. and A.E.B. contributed equally.

S.H.R. and G.S.B. contributed equally.

Dear Editor, The phenotype associated with spontaneous mutation in the tetratricopeptide repeat domain 7A gene (Ttc7) in flaky skin (fsn) mice1 combines gastric hyperplasia, hyperproliferative immune disorder and skin anomalies. All fsn mice progressively develop thick white scales and patchy alopecia that turns into papulosquamous lesions, marked hyperkeratosis and hypergranulosis associated with a dermal mixed inflammatory infiltrate on skin biopsy.2,3 Currently the fsn mouse constitutes a model for human psoriasis vulgaris.3

In humans, TTC7A mutation was recently shown to cause a rare autosomal recessive inherited condition combining an immunodeficiency and an enteropathy of variable intensity (MIM 243150).4,5,6 We observed that some patients with TTC7A deficiency also develop dermatological features. We thus characterized the dermatological features presented by TTC7A‐deficient patients, which were compared with those found in fsn mice.

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