The potential clinical utility of anti-IL-4Rα antagonism (20) is encouraged by the significant overlap observed between dupilumab-regulated markers in AD and those that are dysregulated in keloids, including markers of the Th2 axis, as well as cellular infiltrates (CD3+, CD11c+, FCεR1+), T-cell activation/migration (GZMB, ICOS, CCR7), and the Th17/Th22 (PI3, S100As) pathway (37, 71). The gene discussed is PI3; the disease is keloid.