Because keratinocyte responses and epidermal changes are also hallmarks of inflammatory skin disease and because secondary activation of keratinocytes, including downstream cytokine and chemokine production, are likely products of the sRICA Assay, we evaluated a selection of RORγt-independent genes overexpressed in human psoriasis: cxcl10, il1β, cebpa, il36b (il1f8), s100a12, tgfα, serpinb, il23p19, il23p40, s100a7a, il19, il36g (il1f9), defb4 [7]. This evidence concerns the gene IL36G and psoriasis.