For Psoriasis progression, IL-36γ is the key ingredient in the dermal vascular compartment and is likely to enhance psoriatic skin inflammation by activating endothelial cells and promoting leukocyte recruitment 21; there were also several research pointing toward a critical function of IL-36 in the priming of Th1 cell responses in vitro, and in adaptive immunity in a model of mycobacterial infection in vivo22; some other research suggested a beneficial effect of inhibition from IL-36γ/IL-17C axis-against anti-TNF-induced psoriasis form lesions in patients with inflammatory bowel disease 23. This evidence concerns the gene TNF and psoriasis.