Some authors have speculated that inhibition of TNF or the IL-17/23 axis permits development of T-helper 2 (Th2)–mediated inflammation, which may otherwise be inhibited by Th1/Th17 activity.3,24 Th2-predominant or mixed inflammatory profiles in lesional skin have been described in small case series.25,26 The biological basis for IL-23 inhibitors being associated with the lowest risk of paradoxical eczema is unclear. The gene discussed is IL17A; the disease is Eczematoid dermatitis.