Studies had suggested that the comorbidity of psoriasis and metabolic diseases were due to the excessive production of pro-inflammatory mediators by psoriasis skin lesions [including IL-6, IL-1, IL-23, IL-22, IL-17, vascular endothelial growth factor (VEGF), tumor necrosis factor (TNF)-α, etc.], which could migrate to the systemic circulation, potentially inducing circulatory endothelial dysfunction, increased angiogenesis, systemic insulin resistance, hypercoagulability, and increased oxidative stress. This evidence concerns the gene IL22 and Other metabolic disease.