It is well known that IL-4 is a cytokine that is capable of negatively affecting Th17 lymphocyte function and upstream IL-23 production secreted by antigen-presenting cells; therefore, IL-4/IL-13 inhibition may relieve suppression of the IL-23/IL-17 axis, increasing Th17-mediated inflammation and associated comorbidities like psoriasis, though not all Th17 diseases show this pattern, since ankylosing spondylitis and inflammatory bowel disease are not associated with dupilumab therapy [15]. The gene discussed is IL23A; the disease is ankylosing spondylitis.