Moreover, findings of microarray analysis studying transcriptomes from patients with plaque psoriasis and GPP reflect this IL-1/IL-36 protagonism: expression of IL-1β, IL-36α, IL-36γ, and neutrophil chemokines (CXCL1, CXCL2, CXCL8) was higher, while IL-17A and IFNγ expression was lower in GPP lesions as compared to plaque psoriasis lesions [5]. Here, IL36G is linked to psoriasis vulgaris.