In summary, the findings of this study support that S100A8/A9 and S100A12 do play a role in the pathogenesis of FCE and do not differ between the two main groups of FCE, which supports the theory of CIE and SCL presenting different stages along a spectrum of the same disease process. The gene discussed is S100A12; the disease is congenital non-bullous ichthyosiform erythroderma.