This module includes pro-inflammatory mediators such as IL1β, which is known to stimulate Th17 differentiation [44], and IL1F8, which stimulates pro-inflammatory mediators in fibroblasts [45], but also anti-inflammatory cytokines such as IL-1F5, which actually inhibits inflammatory skin disease [46], as well as the IL1 receptor antagonist (IL1RA). This evidence concerns the gene IL36B and inflammatory skin disease.