The targeted mechanism of action of such monoclonal antibodies (mAbs), as well as chimeric proteins, allows the inhibition of central cytokines that interconnect the numerous psoriasis-related pathways, such as TNF, IL-17, IL-12, and IL23 (Figure 1), without nevertheless the absence of unresponsive patients which is estimated at 30–50% [107]. The gene discussed is IL23A; the disease is psoriasis.