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 IL17A and psoriasis.