Activated and differentiated helper T cell subsets (Th1, Th17, and Th22) and their effector pro-inflammatory cytokine (e.g. TNFα and IL-17A) mediators play a major role in the pathophysiology of psoriasis, promote the synthesis of acute phase proteins and are often associated with extracutaneous and systemic comorbidities (5–8). This evidence concerns the gene IL17A and psoriasis.