Nonetheless, some evidence suggests that interleukin (IL)-17A plays a role in this process: (i) Thus, overexpression of IL-17 in the skin does not only lead to psoriasis but also precipitate bone marrow activation and neutrophil recruitment [14]; (ii) IL-17 producing cells have been shown in the circulation of PsA patients and their number is associated to disease activity in the joints [15]; and (iii) IL-17 inhibition has shown to provide comprehensive effects on skin, entheseal, and joint manifestations of the disease [16, 17]. The gene discussed is IL17A; the disease is psoriasis.