Overall, the detectable expression of 10 out of 11 downstream target genes in severe acute SLL tissue supports the hypothesis that lamellar tissue is responding via a similar IL-17A inflammatory pathway to that identified in human and animal models of auto-inflammatory diseases of the skin and extracutaneous sites, including psoriasis/psoriatic enthesis-arthritis and skin cancer, as well as the wound healing response in human or mouse skin [18, 19, 25]. This evidence concerns the gene IL17A and arthritic joint disease.