According to clinical, histological and molecular markers, selective blockade of IL‐23‐induced IL‐17A leads to complete recovery from psoriasis; nevertheless, IFN‐γ has a role in promoting the release of IL‐23, IL‐1 and chemokines CXCL10 and CXCL11, as well as the expression of dendritic cells, T cells, keratinocytes and endothelial cell adhesion molecules, which can promote inflammatory cells to lesion recruitment of plaques. This evidence concerns the gene IL1B and psoriasis.